Tuesday, June 20, 2006

Sex Worker and Idus In Bangladesh is Vulnerable of HIV/AIDS

Although Bangladesh continues to be a low prevalence area, it is surrounded by high prevalence countries (High prevalence of HIV/AIDS in neighboring India). We however must not adopt a complacent attitude in respect as our country has all the determinants for an explosive outbreak of HIV/AIDS epidemic. Curses of poverty, illiteracy, ignorance, proximity of Bangladesh to the so-called 'Golden Triangle' & high prevalence of STDs, make our country seriously vulnerable. Drug use increases the HIV risk and can start very early-for example, glue-sniffing by youngsters living or working on the streets. The danger of becoming infected with HIV by sharing injecting equipment is well known, and real. Unemployment, slum housing, family fragility, frequent cross-border movement of people, lack of information, unsafe blood transfusion, physical and sexual abuse-that create a "risk environment" of violence for many young people in the region. In addition increased number of migrant workers, unsafe practice in health service, unsafe sex practice etc. movement of population, less use of condom, polygamy, homosexuality, extra-marital relations, further increases the susceptibility.

In Bangladesh, the intravenous drug users (IDU) are the most potential carriers of HIV/AIDS among the vulnerable groups in the country. The fourth round of national HIV and behavioural surveillance report showed that the HIV infection rate among the injection drug users (IDUs) is now 4 per cent, up from 2.5 per cent previously which is just short of the 5 per cent mark of a concentrated epidemic. About 93.4 per cent IDUs in central Bangladesh admitted that they share same syringe while taking drugs. Even they use the same syringe several times for taking drug.

UNCDP estimates that between 500,000 and 1,00,000 people in Bangladesh are addicted to drugs. Although HIV rates are comparatively lower (one per cent) among the sex workers but Sexually Transmitted Infection (STI) rates are still quite high (20 per cent) among this group.

On the other hand, brothel-based female sex workers in Bangladesh report the highest turnover of clients than anywhere in Asia (an average of 18.8 clients per week).

Meanwhile, most of the people of country are unaware about the deadly disease. The 1999-2000 Bangladesh Demographic and Health Survey found that only 31 per cent of married women and 50 per cent of newly married men had heard of AIDS. Over 90 per cent of rickshaw pullers could not identify a single method of HIV prevention.

About 13,000 to 17,000 people are living with the incurable virus in Bangladesh, according to the UNAIDS report 2001.

According to the National AIDS Committee and surveillance team members and experts, the rate is quite alarming as it remains one per cent less than the highest five per cent HIV epidemic index. The rate of HIV/AIDS remains less than one per cent among the other vulnerable groups -- truckers, migrant workers, gay, hijras (hermaphrodites), professional blood donors, heroin smokers and, hotel, brothel and street based commercial sex workers.

Bangladesh is bordered with India, the second largest HIV infected country in the world; the country is therefore at high risk for the HIV epidemic, said Morten Giersing, UNICEF's country representative.

Mohammad Khairul Alam Executive Director ‘Rainbow Nari O Shishu Kallyan Foundation’

24/3 M. C. Roy Lane Nowbabgonj- Section Post Cod- 1211, Dhaka Bangladesh Tel: 88-02-8628908 Mobile: 0171344997 Email: Rainbow.Foundation@gmail.com Web: http://www.plusbangla.com/shaheen

MSS (Master in Social Science) Subject- Social welfare, Dhaka University
Father’s Name : Al-Haz Dr. MD. Abdul Matin
Mother’s Name : Ms. Kadija Matin
Date of Birth : 29th October, 1970
Nationality : Bangladeshi (by birth)

Specialization synopsis

HIV/AIDS program consultant

-Have a sound experience in research and development field. -Good competency in research, planning, monitoring and evaluation; Participated in a number of International Seminars, Training Programs and Workshop. -Smoothly participates in PPME (participatory Planning, Monitoring and Evaluation) -Proficient in Non- Formal Education, Technological Based Education, Gender, HIV/ AIDS Project Proposal writing, Reporting, Project Design, Strategic Planning etc.

Saturday, October 08, 2005

AIDS

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AIDS

Latest News
Study Supports Routine HIV Tests for Fever Patients (09/30/2005, New York Times Syndicate)
POZ Parties May Spread HIV Superstrain (09/29/2005, United Press International)
Scientists Study HIV Drug Resistance Tests (09/27/2005, United Press International)
FDA Approves First Pediatric Generic AIDS Drug for U.S. Marketing (09/19/2005, Food and Drug Administration)
FDA Tentatively Approves Generic Zidovudine Oral Solution (09/08/2005, Food and Drug Administration)
Survey Uncovers Surprising Attitudes Towards HIV Vaccine Research (08/08/2005, National Institute of Allergy and Infectious Diseases)
More News on AIDS
From the National Institutes of Health
HIV Infection and AIDS (National Institute of Allergy and Infectious Diseases)
Overviews
AIDS (Patient Education Institute) - Requires Flash PlayerAlso available in: Spanish
Frequently Asked Questions (FAQs) about HIV and AIDS (National Center for HIV, STD, and TB Prevention)
HIV/AIDS (Mayo Foundation for Medical Education and Research)
JAMA Patient Page: HIV Infection - The Basics (American Medical Association)Also available in: Spanish
Diagnosis/Symptoms
FDA Approves First Oral Fluid Based Rapid HIV Test Kit (Food and Drug Administration)
HIV Antibody Test (American Association for Clinical Chemistry)
OraQuick Rapid HIV-1 Antibody Test (Centers for Disease Control and Prevention)
p24 Antigen Test (American Association for Clinical Chemistry)
Testing HIV Positive – Do I Have AIDS? (AIDSinfo)Also available in: Spanish
Testing Yourself for HIV-1, the Virus that Causes AIDS (Center for Biologics Evaluation and Research)
Treatment
AIDS Drugs Assistance Programs (AIDS Treatment Data Network)
Antiretroviral Drugs (AIDSinfo)Also available in: Spanish
Combination Therapy (AIDS Treatment Data Network)
FDA Approves Two Fixed-Dose Combination Drug Products for the Treatment of HIV-1 Infection (Food and Drug Administration)
HIV and Its Treatment: What You Should Know (AIDSinfo)Also available in: Spanish
HIV/AIDS Treatment Guidelines (AIDSinfo)
HIV: Medicines for People Who Are HIV-Positive (American Academy of Family Physicians)
Patient Assistance Programs - HIV/AIDS Drugs (University of California, San Francisco)
Taking Current Antiretroviral Drugs (New Mexico AIDS Education and Training Center) - Links to PDFAlso available in: Spanish
Treatment of HIV Infection (National Institute of Allergy and Infectious Diseases)
Prevention/Screening
Can I Get HIV from Getting a Tattoo or through Body Piercing? (Centers for Disease Control and Prevention)
Drug Use and HIV (New Mexico AIDS Education and Training Center)Also available in: Spanish
Frequently Asked Questions about HIV Testing (Centers for Disease Control and Prevention)
HIV and AIDS: Are You at Risk? (National Center for HIV, STD, and TB Prevention)Also available in: Spanish
HIV and AIDS: How to Reduce Your Risk (American Academy of Family Physicians)Also available in: Spanish
How to Use a Condom (American Social Health Association)
Alternative Therapy
AIDS Research Center (Bastyr University)
Alternative and Complementary Therapies (New Mexico AIDS Education and Training Center)Also available in: Spanish
Disease Management
CD4 Count (American Association for Clinical Chemistry)
Genotypic Resistance Testing (American Association for Clinical Chemistry)
HIV and Plasma Viral Load Testing (American Academy of Family Physicians)
HIV Resistance Testing (New Mexico AIDS Education and Training Center) - In English and SpanishAlso available in: Spanish
HIV Viral Load (American Association for Clinical Chemistry)
Specific Conditions
HIV: What Is Acute HIV Syndrome? (American Academy of Family Physicians)
Neurological Complications of AIDS (National Institute of Neurological Disorders and Stroke) - Short Summary
Related Issues
Can I Get HIV from Mosquitoes? (Centers for Disease Control and Prevention)
Drug Abuse and AIDS (National Institute on Drug Abuse)
FDA Approves Sculptra for HIV Patients (Food and Drug Administration)
Occupational Exposure to HIV: Advice for Health Care Workers (American Academy of Family Physicians)Also available in: Spanish
Oral Polio Vaccine and HIV / AIDS (National Immunization Program)
Sex Differences in HIV/AIDS (Society for Women's Health Research)
Financial Issues
Medicaid and Acquired Immunodeficiency Syndrome (AIDS) and Human Immunodeficiency Virus (HIV) Infection (Centers for Medicare & Medicaid Services)
Clinical Trials
ClinicalTrials.gov: Acquired Immunodeficiency Syndrome (National Institutes of Health)
ClinicalTrials.gov: HIV Infections (National Institutes of Health)
HIV/AIDS Clinical Trials (AIDSinfo)
TrialScope (University of California, San Francisco)
What Is an AIDS Clinical Trial? (AIDSinfo)Also available in: Spanish
Genetics
Scientists Discover Key Genetic Factor in Determining HIV/AIDS Risk (National Institute of Allergy and Infectious Diseases)
Research
African Americans: Answers about HIV Vaccine Research (01/01/2005, National Institute of Allergy and Infectious Diseases) - Links to PDF
Analysis Shows Infants of Mothers Infected with HIV Face Nearly Constant Risk for HIV Infection for Duration of Breastfeeding (06/16/2004, National Institute of Child Health and Human Development)
Estimating Outcome in Patients with HIV-Related Lymphoma (08/16/2005, American College of Physicians)
HIV Lipodystrophy: Rosiglitazone or Metformin? (09/06/2005, American College of Physicians)
HIV Patients Get Long-Term Boost with Short, Intermittent Drug Regimen (04/26/2004, National Institute of Allergy and Infectious Diseases)
HIV Vaccines Explained--Making HIV Vaccines a Reality (National Institute of Allergy and Infectious Diseases) - Links to PDFAlso available in: Spanish
How HIV Causes AIDS (11/01/2004, National Institute of Allergy and Infectious Diseases)
International Trial of Two Microbicides Begins (02/11/2005, National Institute of Allergy and Infectious Diseases)
Primary HIV Infection Associated with Oral Transmission (04/01/2003, National Center for HIV, STD, and TB Prevention)
Scientists Discover Enzyme Crucial to HIV Replication (10/28/2004, National Institute of Allergy and Infectious Diseases)
Scientists Discover HIV Medication May Preserve Bone (08/01/2004, National Institute of Arthritis and Musculoskeletal and Skin Diseases)
Scientists Discover New Approaches to Manipulating AIDS Virus (08/16/2004, National Cancer Institute)
Dictionaries/Glossaries
Glossary of HIV/AIDS-Related Terms (AIDSinfo)Also available in: Spanish
Directories
Guide to NIH HIV/AIDS Information Services (National Library of Medicine)
Organizations
AIDS Education Global Information System
AIDS Treatment Data Network
AIDSinfo (Dept. of Health and Human Services)
American Social Health Association
CDC Divisions of HIV/AIDS Prevention (National Center for HIV, STD, and TB Prevention)Also available in: Spanish
National Institutes of Health, Office of AIDS Research
NIAID Division of AIDS (National Institute of Allergy and Infectious Diseases)
Project InformAlso available in: Spanish
Statistics
Basic HIV/AIDS Statistics (Centers for Disease Control and Prevention)
Eliminate Disparities in HIV and AIDS (Centers for Disease Control and Prevention, Office of Minority Health)
HIV/AIDS Surveillance Report (Centers for Disease Control and Prevention)
Percent of Adults Aged 18 Years and Over Who Had Ever Been Tested for HIV: United States, 1997 - 2002 (National Center for Health Statistics)
Rates of US HIV/AIDS Diagnoses Are Steady; Racial Disparities Persist (Centers for Disease Control and Prevention)
Statistics and Trends (National Center for Infectious Diseases)
Children
HIV and AIDS (Nemours Foundation)
Teenagers
HIV and AIDS (Nemours Foundation)
HIV Infection in Adolescents and Young Adults in the U.S. (National Institute of Allergy and Infectious Diseases)
How Do People Get AIDS? (Nemours Foundation)Also available in: Spanish
Men
What Do You Know about Men's Health? Sexually Transmitted Diseases (STDs) and HIV/AIDS in Men (National Women's Health Information Center)
Women
HIV Infection in Women (National Institute of Allergy and Infectious Diseases)
Women and HIV/AIDS (National Women's Health Information Center)Also available in: Spanish
Women and HIV/AIDS in the United States (Henry J. Kaiser Family Foundation) - Links to PDF
Seniors
Older People and HIV (New Mexico AIDS Education and Training Center)Also available in: Spanish
>>http://www.nlm.nih.gov/medlineplus/aids.html#diagnosissymptoms











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How to Use a Condom - Instructions for Male Condoms

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How to Use a Condom
Instructions for Male Condoms > Without Pictures

Treat condoms gently and keep them out of the sun. With latex condoms, never use lotions, baby oil, Vaseline®: or cold cream -- the oil in these products weakens the condom. If you use a lubricant, use one made with water (such as K-Y®: jelly or glycerin). Regular use of spermicidal lubricants should be avoided as they may cause skin irritation. Put the condom on before the penis touches the vagina, mouth or anus.

Hold the condom by the tip to squeeze out the air. Leave some space at the tip to hold the ejaculate (cum). Unroll the condom all the way over the erect penis. After sex, the man should hold the condom at the rim and pull out slowly while the penis is still hard.

Use a new condom if you want to have sex again or if you want to have sex in a different place (for example, in the anus and then in the vagina).











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How to Use a Condom

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How to Use a Condom
Do's and Don'ts

DO's:

DO use only latex or polyurethane (plastic) condoms.
DO keep condoms in a cool, dry place.
DO put the condom on an erect (hard) penis before there is any contact with a partner's genitals.
DO use plenty of water-based lubricant (like KY Jelly® or Astroglide®) with latex condoms. This reduces friction and helps prevent the condom from tearing.
DO squeeze the air out of the tip of the condom when rolling it over the erect penis. This allows room for the semen (cum).
DO hold the condom in place at the base of the penis before withdrawing (pulling out) after sex.
DO throw the condom away after it's been used.
DON'Ts:

DON'T use out of date condoms. Check the expiration date carefully. Old condoms can be dry, brittle or weakened and can break more easily.
DON'T unroll the condom before putting it on the erect penis.
DON'T leave condoms in hot places like your wallet or in your car.
DON'T use oil-based products, like baby or cooking oils, hand lotion or petroleum jelly (like Vaseline®) as lubricants with latex condoms. The oil quickly weakens latex and can cause condoms to break.
DON'T use your fingernails or teeth when opening a condom wrapper. It's very easy to tear the condom inside. If you do tear a condom while opening the wrapper, throw that condom away and get a new one.
DON'T reuse a condom. Always use a new condom for each kind of sex you have.
DON'T regularly use lubricants with spermicide called nonoxynol-9 ("N-9") as they may cause skin irritation or tiny abrasions that make the genital skin more susceptible to STDs.


>>http://www.ashastd.org/condom/condom_male_nopics.cfm









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HIV/AIDS Symptoms

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HIV/AIDS Symptoms

It's one of the most common questions we are asked on the hotline: "What are the symptoms of AIDS?" In order to answer that question, we have to keep in mind several different issues:

Symptom-Free Period
Becoming infected with HIV and becoming sick from AIDS are two different events (read about the difference between HIV and AIDS). For most people, it takes many years from the time someone is infected with HIV to the time that they develop symptoms of AIDS. Some people get sick sooner and others stay well longer, especially with treatment. However, there is almost always a significant period of time after infection when an HIV-positive individual will have no symptoms at all -- often 10 years or more.

Keeping in mind the two separate events (becoming HIV-infected vs. actually developing AIDS) can help you to remember that there are also two separate time periods when someone may show symptoms related to HIV-infection.

Acute Viral Syndrome
The first time period is during the first few weeks after infection from HIV. Some people who are newly infected may develop flu-like symptoms within the first month or so after getting HIV. These early symptoms can feel very much like the flu (fever, headache, weakness, fatigue, body aches, etc.), and they can be mild or severe. The flu-like symptoms typically last for only about week, and then go away on their own. Acute Viral Syndrome is not an ongoing condition that lasts for weeks and weeks or that comes and goes over a long period of time. In addition, it's important to know that:


Not everyone who is infected with HIV will experience these early, flu-like symptoms of Acute Viral Syndrome. Many people will have no symptoms at all until years after infection.


The symptoms of Acute Viral Syndrome are the same as the symptoms for the flu and many other illnesses. If you have these symptoms right after a possible exposure to HIV, it does not mean you that have the virus, or even that you probably have it. The only way to find out if you have HIV is to get an HIV test.

Symptoms of AIDS
The other time when someone may have symptoms related to HIV is much later in their illness, once their body's immune system has been damaged by the virus and they are starting to become sick with AIDS. As mentioned before, this is usually years after they've been infected by HIV.

Because AIDS is a disorder of the immune system, it makes people sick by making their bodies vulnerable to a wide variety of illnesses (opportunistic infections), each with its own symptoms. For this reason, there isn't a simple checklist of "AIDS symptoms" that we can give you. Two people who are both sick with AIDS can have completely different sets of symptoms (or even no symptoms at all).

If you have symptoms that are bothering you or that aren't going away, your best option is to be checked by a health care provider. Any symptom that could be a sign of AIDS could also be a sign of something else. Again, the only way to know if you are HIV-positive is to take an HIV test.

If you live in Florida and you have further questions or concerns about HIV/AIDS symptoms, or if you need a referral to an HIV test site, please call the Florida HIV/AIDS Hotline (1-800-FLA-AIDS) or send e-mail to hivhotline@211bigbend.org.

If you live outside of Florida, visit The Body to find an AIDS hotline near you.












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How can I tell if I'm infected with HIV?

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How can I tell if I'm infected with HIV?
What are the symptoms?
The only way to know if you are infected is to be tested for HIV infection. You cannot rely on symptoms to know whether or not you are infected. Many people who are infected with HIV do not have any symptoms at all for many years.

The following may be warning signs of HIV infection:

rapid weight loss
dry cough
recurring fever or profuse night sweats
profound and unexplained fatigue
swollen lymph glands in the armpits, groin, or neck
diarrhea that lasts for more than a week
white spots or unusual blemishes on the tongue, in the mouth, or in the throat
pneumonia
red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids
memory loss, depression, and other neurological disorders
However, no one should assume they are infected if they have any of these symptoms. Each of these symptoms can be related to other illnesses. Again, the only way to determine whether you are infected is to be tested for HIV infection. For information on where to find an HIV testing site, visit the National HIV Testing Resources Web site at http://www.hivtest.org or call CDC-INFO 24 Hours/Day at1-800-CDC-INFO (232-4636), 1-888-232-6348 (TTY), in English, en Español.

You also cannot rely on symptoms to establish that a person has AIDS. The symptoms of AIDS are similar to the symptoms of many other illnesses. AIDS is a medical diagnosis made by a doctor based on specific criteria established by the CDC. For more information refer to the Morbidity and Mortality Weekly Report “ 1993 Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults ” at http://www.cdc.gov/mmwr/preview/mmwrhtml/00018871.htm.

If you would like more information or have personal concerns, call CDC- INFO 24 Hours/Day at1-800-CDC- INFO (232-4636 ), 1-888-232-6348 (TTY), in English, en Español.











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What are the symptoms of HIV infection?

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What are the symptoms of HIV infection?

September 2004


How can I tell if I have HIV?

The first symptoms of HIV infection can resemble symptoms of common cold or flu viruses. The symptoms of early infection can also be similar to the symptoms of other sexually transmitted diseases and other infections such as "mono" or hepatitis, which are much more commonly and more easily transmitted. Stress and anxiety can also produce symptoms in some people, even though they do not have HIV.

Some people who contract HIV experience very strong symptoms, but others experience none at all. Those who do have symptoms generally experience fever, fatigue, and, often, rash. Other common symptoms can include headache, swollen lymph nodes, and sore throat. These symptoms can occur within days or weeks of the initial exposure to the virus during a period called primary or acute HIV infection.

Because of the nonspecific symptoms associated with primary or acute HIV infection, symptoms are not a reliable way to diagnose HIV infection. Testing for HIV antibodies is the only way to know whether you have been infected; however, the HIV antibody test only works after the infected person's immune system develops antibodies to HIV. During the "window period" between the initial infection and the period in which antibodies are detectable (which can be from 2 weeks to 6 months, but is usually 3 months), standard HIV testing is ineffective.

If you are concerned that you may have recently acquired HIV and have symptoms described above, see a doctor. A doctor or other health care professional can help determine whether you may be infected with HIV or another infection. If HIV infection is suspected, he or she may perform a Polymerase Chain Reaction (commonly called "PCR") test to determine whether HIV is present in the blood.

Once the primary or acute infection is over, most people do not experience any visible symptoms for another 8-10 years. Left untreated, the immune system becomes increasingly weaker and the disease progresses to AIDS. The next symptoms experienced by individuals infected with the virus are often associated with the "opportunistic infections" that target individuals with AIDS such as pneumonia, tuberculosis, and toxoplasmosis.


How can I tell if someone else has HIV?

There is no way to know for sure if someone else has HIV. Many people with HIV look perfectly healthy. Other people who are sick with HIV may have symptoms that are identical to other common illnesses. You cannot tell by looking whether someone is HIV positive. The only way to know for sure is if someone tells you. It is important to consider how well you know someone and how much you trust them when talking about sex and HIV.













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Tuesday, October 04, 2005

10 Essential Food Safety Tips For AIDS Sufferers

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10 Essential Food Safety Tips For AIDS Sufferers
by: Terry Nicholls

Persons with Acquired Immunodeficiency Syndrome (AIDS) are especially susceptible to illness from food-borne pathogens. Because they're at higher risk for severe illness or death, affected persons must be vigilant when handling and cooking foods. Here are some recommendations to help prevent bacterial food-borne illness.

1. When shopping for raw and cooked perishable foods, be sure the food is being stored at a safe temperature in the store. Don't select perishable food from a non-refrigerated aisle display. Never choose packages which are torn or leaking.

2. When ordering food from the deli department, be sure the clerk washes his hands between handling raw and cooked items or puts on new plastic gloves. Don't buy cooked ready-to-eat items which are touching raw items or are displayed in the same case.

3. Don't buy cans that are dented, leaking, or bulging; food in cracked glass jars; or food in torn packaging. Tamper- resistant safety seals should be intact. Safety buttons on metal lids should be down and should not move or make a clicking noise when pushed. Do not use any product beyond its expiration date!

4. Immediately refrigerate or freeze perishable foods after transporting them home. Make sure thawing juices from meat and poultry do not drip on other foods. Leave eggs in their carton for storage and don't place them in the door of the refrigerator. Keep the refrigerator clean.

5. Food stored constantly at 0 °F will always be safe. Only the quality suffers with lengthy storage. It's of no concern if a product date expires while the product is frozen. Freezing keeps food safe by preventing the growth of micro- organisms that cause both food spoilage and food-borne illness. Once thawed, however, these microbes can again become active so handle thawed items as any perishable food.

6. Store canned foods and other shelf stable products in a cool, dry place. Never put them above the stove, under the sink, in a damp garage or basement, or any place exposed to high or low temperature extremes.

7. Wash hands, utensils, can openers, cutting boards, and countertops in hot, soapy water before and after coming in contact with raw meat, poultry, or fish.

8. Many cases of food-borne illness are caused by take-out, restaurant, and deli-prepared foods. Avoid the same foods when eating out as you would at home. Meat, poultry, and fish should be ordered well done; if the food arrives undercooked, it should be sent back.

9. Wash cutting boards with hot, soapy water after each use; then rinse and air dry or pat dry with fresh paper towels. Non-porous acrylic, plastic, or glass boards and solid wood boards can be washed in an automatic dishwasher (laminated boards may crack and split).

10. Do not eat raw or undercooked meat, poultry, fish, or eggs. For people with AIDS, the most important thing is to use a meat thermometer to be sure meat, fish, eggs, and casseroles reach at least 160 °F. Roast whole poultry to 180 °F; poultry breasts to 170 °F. When reheating foods in the microwave, cover and rotate or stir foods once or twice during cooking and check the food in several spots with a thermometer.

Copyright (c) Terry Nicholls. All Rights Reserved.

About The Author


Terry Nicholls is the author of the eBook "Food Safety: Protecting Your Family From Food Poisoning". For more tips like these, and to learn more about his book, visit his website at http://tinyurl.com/3fr2t
yourguides@cogeco.ca















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AIDS 101- What You Absolutely Need to Know

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AIDS 101- What You Absolutely Need to Know
By Mansi Aggarwal

Introduction

Due both to the stigma and the awareness program attached with it, now AIDS has become a common household term. There are very less people who actually know that the exact word is Acquired Immune Deficiency Syndrome, AIDS in short. Because of the morbidity and mortality attached and also because of the ignorance about it there are lots and lots of myths against this deadly disease. This alone shows the anxiety and concern of the general mass.

History

The virus for this disease is thought to have transmitted from simian monkeys in the forests of Africa to humans and from there it traveled to USA and different countries. It was brewing in the bodies till in 1981 in USA the Center for Disease Control and prevention (CDC) recognized it for the first time and reported that there was an unexplained occurrence of an unusual pneumonia in a few homosexuals. Soon the disease was to be found in intravenous drug users. But it was only in 1983 that the causative virus was isolated from a patient and then further classified. Obviously because of the ignorance initially the information was confined to only certain specific institutions in the early 1980s. Then as the disease became more prevalent and showed its mortality pattern more and more people became aware of this disease. Today it’s a topic of concern for every type of doctor be it a family physician, obstetrician, dentist, dermatologist or any other field.

HIV and AIDS

AIDS is a disease, as the name suggests, in which the person over a period of time loses his power of immunity to fight infections and hence he is a prey to a host of infections which otherwise wont have occurred. The causative organism is a virus called the Human Immunodeficiency Virus. On gaining entry into the body of a subject through another patient’s body fluids such as blood, blood products, semen, etc. the virus remains in the lymphatic system and gets replicated. Then over a period of years it reduces the body’s immune system.

Current problem

The problem is so severe that according to CDC, till 2003 the number of AIDS cases in USA are 1.2 million and the number are still increasing and 40,000 new cases get infected each year in whole of USA.

Diseases associated with aids

There are many different diseases associated with this disease ranging from all types of bacterial infections to viral infections and other protozoal and helminthic infections.

Management

The disease is managed by a whole lot of drugs because of the inability of the scientists to develop a vaccine against it. The drugs against it are basically divided into two types. One type prevents against the possible development of the potential bacterial, viral and helminthic infections and the other group helps in the killing and preventing replication of HIV. The first group has drugs such as trimethoprim sulfamethoxazole, clarithromycin, amphotericin, fluconazole, etc. The latter group has antiviral drugs such as zidovudine, didanosine, saquinavir, indinavir, enfuvirtide, etc.

Prevention

Till there are no effective vaccines available prevention is the best cost effective treatment available. Adherence to universal precautions meaning that every body fluid from a patient is considered to be infected from HIV until proven otherwise should be practiced. Also there are various institutions and organizations both governmental and non-governmental involved in creating awareness throughout the world.

Mansi gupta writes about aids topics.

Article Source: http://EzineArticles.com/










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HIV

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HIV

Human immunodeficiency virus

Stylized rendering of a cross section
of the human immunodeficiency virus
Virus classification
Group: Group VI (ssRNA-RT)
Family: Retroviridae
Genus: Lentivirus
Species: Human immunodeficiency virus 1
Species: Human immunodeficiency virus 2

The human immunodeficiency virus, commonly called HIV, is a retrovirus that primarily infects vital components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. It also directly and indirectly destroys CD4+ T cells. As CD4+ T cells are required for the proper functioning of the immune system, when enough CD4+ cells have been destroyed by HIV, the immune system barely works, leading to AIDS. HIV also directly attacks certain human organs, such as the kidneys, the heart and the brain leading to acute renal failure, cardiomyopathy, dementia and encephalopathy. Many of the problems faced by people infected with HIV results from the failure of the immune system to protect them from certain opportunistic infections and cancers.

HIV is transmitted through penetrative (anal or vaginal) and oral sex; blood transfusion; the sharing of contaminated needles in health care settings and through drug injection; and, between mother and infant, during pregnancy, childbirth and breastfeeding.

AIDS is thought to have originated in sub-Saharan Africa during the twentieth century and it is now a global epidemic. At the end of 2004, UNAIDS estimated that nearly 40 million people were currently living with HIV [1]. The World Health Organization estimated that the AIDS epidemic had claimed more than 3 million people and that 5 million people had acquired HIV in the same year.

Contents [hide]
1 Introduction
2 The clinical course of HIV-1 infection
2.1 Primary Infection
2.2 Clinical Latency
2.3 The declaration of AIDS
3 HIV Structure and Genome
3.1 Structure
3.2 HIV genome organisation and HIV protein function
3.2.1 gag
3.2.2 pol
3.2.3 env
3.2.4 tat
3.2.5 rev
3.2.6 nef
3.2.7 vif
3.2.8 vpr
3.2.9 vpu
3.2.10 tev
4 HIV tropism
5 Life cycle of HIV
5.1 Viral entry to the cell
5.2 Viral replication and transcription
5.3 Viral assembly and release
5.3.1 Immature form
5.3.2 Mature form
6 Genetic variability of HIV
7 Treatment
8 Transmission and Epidemiology
8.1 Sub-Saharan Africa
8.2 North Africa and the Middle East
8.3 South and South-East Asia
8.4 East Asia
8.5 Eastern Europe and Central Asia
8.6 Western Europe
8.7 North America
8.8 Caribbean
8.9 Latin America
8.10 Oceania
9 References
10 See also
11 External links




Introduction
In 1983, scientists in France led by Luc Montagnier, first discovered the virus that causes AIDS [2]. They called it lymphadenopathy-associated virus (LAV). A year later, Robert Gallo of the United States, confirmed the discovery of the virus, and they named it human T lymphotropic virus type III (HTLV-III) [3]. In 1986, both names were dropped in favour of the term human immunodeficiency virus (HIV) [4].

HIV is a member of the genus lentivirus [5], part of the family of retroviridae [6]. Lentiviruses have many common morphologies and biological properties. Many species are infected by lentiviruses, which are characteristically responsible for long duration illnesses associated with a long period of incubation [7]. Lentiviruses are transmitted as single-stranded negatively-sensed enveloped RNA viruses. Upon infection of the target-cell, the viral RNA genome is converted to double-stranded DNA by a virally encoded reverse transcriptase which is present in the virus particle. This viral DNA is then integrated into the cellular DNA for replication using cellular machinery. Once the virus enters the cell, two pathways are possible: either the virus becomes latent and the infected cell continues to function or the virus becomes active, replicates and a large number of virus particles are liberated which can infect other cells.

Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is the more virulent and easily transmitted, and is the source of the majority of HIV infections throughout the world; HIV-2 is largely confined to west Africa [8]. Both species originated in west and central Africa, jumping from primates to humans in a process known as zoonosis. HIV-1 has evolved from a simian immunodeficiency virus (SIVcpz) found in the chimpanzee subspecies, Pan troglodyte troglodyte [9]. HIV-2 crossed species from a different strain of SIV, found in sooty mangabeys, an old world monkey of Guinea-Bissau [10].


The clinical course of HIV-1 infection

Figure 1. Graph showing HIV virus and CD4+ levels over the course of an untreated infectionInfection with HIV-1 is associated with a progressive loss of CD4+ T-cells. This rate of loss can be measured and is used to determine the stage of infection. The loss of CD4+ T-cells is linked with an increase in viral load. The clinical course of HIV-infection generally includes three stages: primary infection, clinical latency and AIDS (Figure 1). HIV plasma levels during all stages of infection range from just 50 to 11 million virions per ml [11].


Primary Infection
Primary, or acute infection is a period of rapid viral replication that immediately follows the individuals exposure to HIV. During primary HIV infection, most individuals (80 to 90 %) develop an acute syndrome characterised by flu-like symptoms of fever, malaise, lymphadenopathy, pharyngitis, headache, myalgia, and sometimes a rash [12]. Within an average of three weeks after transmission of HIV-1, a broad HIV-1 specific immune response occurs that includes seroconversion. Because of the nonspecific nature of these illnesses, it is often not recognized as a sign of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. Since not all patients develop it, and since the same symptoms can be caused by many other common diseases, it cannot be used as an indicator of HIV infection. However, recognizing the syndrome is important because the patient is much more infectious during this period.


Clinical Latency
As a result of the strong immune defence, the number of viral particles in the blood stream declines and the patient enters clinical latency (Figure 1). Clinical latency is variable in length and can vary between two weeks and 20 years. During this phase HIV is active within lymphoid organs where large amounts of virus become trapped in the follicular dendritic cells (FDC) network early in HIV infection. The surrounding tissues that are rich in CD4+ T-cells also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who have entered into this phase are still infectious.


The declaration of AIDS
AIDS is the most severe manifestation of infection with HIV. Acute HIV infection progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later, to AIDS, which is identified on the basis of certain infections. In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introduced a staging system for patients infected with HIV-1. This was updated in September 2005. Most of these conditions are opportunistic infections that can be easily treated in healthy people.

Stage I: HIV disease is asymptomatic and not categorized as AIDS
Stage II: include minor mucocutaneous manifestations and recurrent upper respiratory tract infections
Stage III: includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis or
Stage IV includes toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi's sarcoma; these diseases are used as indicators of AIDS.
For more details on this topic, see WHO Disease Staging System for HIV Infection and Disease.
In the USA, the definition of AIDS is goverened by the Centers for Disease Control and Prevention (CDC). In 1993, the CDC expanded their definition of AIDS to include healthy HIV positive people with a CD4 positive T cell count of less than 200 per µl of blood. The majority of new AIDS cases in the United States are reported on the basis of a low T cell count in the presence of HIV infection.

For more details on this topic, see CDC Classification System for HIV Infection.
Many factors such as host susceptibility and immune function [13][14][15], health care and co-infections [16][17][18], as well as factors relating to the viral strain [19][20] may affect the rate of progression to AIDS. Thus, following infection with HIV-1, the rate of clinical disease progression varies enormously between individuals.

For more details on this topic, see HIV Disease Progression Rates.

HIV Structure and Genome

Structure

Figure 2. Diagram of the HIV virus

Figure 3. Diagram of the HIV genome
HIV is different in structure from previously described retroviruses. It is around 120 nm in diameter (120 billionths of a meter; around 60 times smaller than a red blood cell) and roughly spherical.

HIV-1 is composed of two copies of single-stranded RNA enclosed by a conical capsid comprising the viral protein p24, typical of lentiviruses (Figure 3). This is in turn surrounded by a plasma membrane of host-cell origin. The single-strand RNA is tightly bound to the nucleocapsid proteins, p7 and enzymes that are indispensable for the development of the virion, such as reverse transcriptase and integrase. The nucleocapsid (p7 and p6) associates with the genomic RNA (one molecule per hexamer) and protects the RNA from digestion by nucleases. A matrix composed of an association of the viral protein p17 surrounds the capsid, ensuring the integrity of the virion particle. Also enclosed within the virion particle are vif, vpr, nef, p7 and viral protease (Figure 2). The envelope is formed when the capsid buds from the host protein, taking some of the host-cell membrane with it. The envelope includes the glycoproteins gp120 and gp41, which are derived from the gp160 precursor; gp41 is a transmembrane protein that is covalently linked to gp120 [21].


HIV genome organisation and HIV protein function
HIV has several major genes coding for structural proteins that are found in all retroviruses, and several nonstructural ('accessory') genes that are unique to HIV.


gag
Group specific antigen (gag)-derived proteins make up the cone-shaped viral capsid (p24, a 24-kilodalton protein), the nucleocapsid proteins (p6 and p7) and a matrix protein (p17).


pol
A gene that codes for the viral enzymes. The most important of which is the reverse transcriptase which performs the unique reverse transcription of the viral RNA into double-stranded DNA. The latter is integrated into the genome of the host, which means into a chromosome of an infected cell of an HIV-positive person by the pol-encoded integrase. Also, pol encodes a specific viral protease. This enzyme cleaves gag- and gag-pol-derived proteins into functional proteins.


env
Codes for the envelope proteins. The proteins derived from env are the surface (gp120) and a transmembrane (gp41) proteins. They are located at the outer part of the virus particle and enable the virus to attach to and fuse with the target cells to initiate the infectious cycle. The gene product has a knob-like structure.


tat

Figure 4. Molecular modeling of Tat. Region I is red; region II (cysteine-rich region) is orange; region III is yellow; region IV (basic region) is green; region V is light blue; and region VI is blue (Click image for more details).
tat (Trans-Activator of Transcription) codes for a protein Tat, which consists of between 86 and 101 amino acids depending on the subtype [22][23] (Figure 4). The HIV RNA initially has a hairpin-structured portion which prevents full transcription occurring. However, a small number of RNA transcripts will be made, which allow the Tat protein to be produced. Tat binds to and phophorylates cellular factors, eliminating the effect of the hairpin RNA structure and allowing transcription of the HIV DNA [24]. This itself increases the rate of transcription, providing a positive feedback cycle. This in turn allows HIV to have an explosive response once a threshold amount of Tat is produced, a useful tool for defeating the body's response. Despite the lack of a signal sequence, Tat is released by infected cells and is found in detectable levels (more than 40nM) in the culture supernatants of cells infected with HIV-1, and in the sera of HIV-1 infected patient’s [25]. It is also efficiently taken up by a variety of HIV-1 uninfected cells. Extracellular Tat has many functions that are thought to play a major role in enabling HIV to escape immune surveillance and to act as a viral toxin in AIDS pathology. One such role of Tat is in the apoptosis of uninfected naive bystander T cells, contributing to the progressive loss of these cells and the progression towards AIDS [26].


rev
rev (Regulator of Virion) codes for Rev, a protein that allows fragments of HIV mRNA that contain a Rev Response Unit (RRE) to be exported from the nucleus to the cytoplasm. In the absence of rev, RNA splicing machinery in the nucleus quickly splices the RNA so that only the smaller, regulatory proteins can be produced; in the presence of rev, RNA is exported from the nucleus before it can be spliced, so that the structural proteins and RNA genome can be produced. Again, this mechanism allows a positive feedback loop to allow HIV to overwhelm the host's defenses, and provides time-dependant regulation of replication (a common process in viral infections) [27].


nef
nef (Negative Regulatory Factor) codes for Nef. The expression of Nef early in the viral life cycle ensures T cell activation and the establishment of a persistent state of infection, two basic attributes of HIV infection. Nef also promotes the survival of infected cells by downmodulating the expression of several surface molecules important in host immune function. These include major histocompatibility complex-I (MHC I) and MHC II present on antigen presenting cells (APCs) and target cells, and CD4 and CD28 present on CD4+ T cells. One group of patients in Sydney were infected with a nef-deleted virus and took much longer than expected to progress to AIDS [28]. A nef-deleted virus vaccine has not been trialed in humans and has failed in nonhuman animals.


vif
vif (Viral Infectivity Factor) codes for a 23-kilodalton protein, Vif. Vif is essential for viral replication. The exact role of Vif is as yet unclear [29]. However, it is thought that vif helps the virus to infect other cells after it leaves a host cell; Vif appears to be involved in determining how the RNA genome and Gag protein bind to each other, and inhibits a cellular protein that modifies RNA.


vpr
vpr (Viral Protein R) codes for a 10-kilodalton protein, Vpr. Vpr plays an important role in regulating nuclear import of the HIV-1 pre-integration complex, and is required for virus replication in non-dividing cells. Vpr also induces cell cycle arrest in proliferating cells, which can result in immune dysfunction [30].


vpu
vpu (Viral Protein U) codes for Vpu. Vpu is involved in viral budding, enhancing virion release from the cell. In HIV-2, this gene is called vpx.


tev
This codes for a a chimeric Tat–Env–Rev fusion protein that has Tat transactivation activity but low detectable Rev activity. Only present in a few HIV-1 isolates (Figure 3).


HIV tropism
The term viral tropism refers to the cell type that the virus infects and replicates in. HIV can infect a variety of cells such as CD4+ helper T-cells and macrophages that express the CD4 molecule on its surface. HIV-1 entry to macrophages and T helper cells is mediated not only through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells but also with its chemokine coreceptors. Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the beta-chemokine receptor CCR5 for entry and are thus able to replicate in macrophages and CD4+ T-cells. The normal ligands for this receptor, RANTES, macrophage inflammatory protein (MIP)-1-beta and MIP-1-alpha, are able to suppress HIV-1 infection in vitro. This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV disease. They appear to be the first cells infected by HIV and perhaps the very source of HIV production when CD4+ cells are markedly depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce copious amounts of virus. T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4+ T-cells as well as in macrophages and use the alpha-chemokine receptor, CXCR4, for entry. The alpha-chemokine, SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down regulating the expression of CXCR4 on the surface of these cells. Viruses that use only the CCR5 receptor are termed R5, those that only use CXCR4 are termed X4, and those that use both, X4R5. However, the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection [31].

HIV can also infect dendritic cells [32].


Life cycle of HIV

Figure 5. The HIV replication cycle

Figure 6. The immature and mature forms of HIV

Viral entry to the cell
The interaction between the gp120, coreceptor and CD4 provokes conformational changes in gp120 that exposes a previously buried portion of the transmembrane glycoprotein, gp41, and allows access of the V3 loop of gp120 to the coreceptor. gp41 causes the fusion of the viral envelope and the host-cell envelope, allowing the capsid to enter the target cell. The exact mechanism by which gp41 causes the fusion is still largely unknown [33][34].

Once HIV has bound to the CD4+ T-cell a viral protein known as gp41 penetrates the cell membrane and the HIV RNA and various enzymes including but not limited to reverse transcriptase, integrase and protease are injected into the cell.


Viral replication and transcription
Once the viral capsid has entered the cell, an enzyme called reverse transcriptase liberates the single-stranded (+)RNA from the attached viral proteins and copies it into a negatively sensed viral complementary DNA of 9 kb pairs (cDNA) (Figure 5). This process of reverse transcription is extremely error prone and it is during this step that mutations (such as drug resistance) are likely to arise. The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). This new vDNA is then transported into the nucleus. The integration of the proviral DNA into the host genome is carried out by another viral enzyme called integrase. This is called the latent stage of HIV infection [35].

To actively produce virus, certain transcription factors need to be present in the cell. The most important is called NF-kB (NF Kappa B) and is present once the T cells becomes activated. This means that those cells most likely to be killed by HIV are in fact those currently fighting infection.

The production of the virus is regulated, like that of many viruses. Initially the integrated provirus is copied to mRNA which is then spliced into smaller chunks. These small chunks produce the regulatory proteins Tat (which encourages new virus production) and Rev. As Rev accumulates it gradually starts to inhibit mRNA splicing [36]. At this stage the structural proteins Gag and Env are produced from the full-length mRNA. Additionally the full-length RNA is actually the virus genome, so it binds to the Gag protein and is packaged into new virus particles.

Interestingly, HIV-1 and HIV-2 appear to package their RNA differently; HIV-1 will bind to any appropriate RNA whereas HIV-2 will preferentially bind to the mRNA which was used to create the Gag protein itself. This may mean that HIV-1 is better able to mutate (HIV-1 causes AIDS faster than HIV-2 and is the majority species of the virus).


Viral assembly and release
The final step of the viral cycle is the assembly of new HIV-1 virions, begins at the plasma membrane of the host cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120. These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. Maturation either occurs in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases (proteinases) cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion [37]. This step can be inhibited by drugs. The virus is then able to infect another cell. There are two forms of the virus:


Immature form
When the virus leaves the cell it is not infectious and the inner part of the virus particle contains a spherical core (stains dark on electron micrographs). There are spikes on the outer membrane that are the Env proteins (gp120 and gp41) (Figure 6). Sometimes a virus can be seen during the process of budding, when it looks like a dark arc sitting under the cell membrane. The Env proteins link together in groups of three (trimers).


Mature form
Once the virus protease has cleaved the gag proteins, the core rearranges into a truncated cone (like a traffic cone sliced at an angle across the top). Some reports also show a small filament linking the core to the membrane. The envelope spikes are often much rarer on mature particles, because they are easily dislodged. It is the mature conical core that makes HIV easily identifiable.


Genetic variability of HIV

Figure 7. The phylogenetic tree of the SIV and HIV viruses (click on image for a detailed description).

Figure 8. Map showing HIV-1 subtype prevalence. The bigger the pie chart, the more infections are present.
One of the major characteristics of HIV is its high genetic variability as a result of its fast replication cycle and the high error rate and recombinogenic properties of reverse transcriptase. This means that different genomic combinations may be generated within an individual who is infected by genetically different HIV strains. Recombination results when a cell is simultaneously infected by two different strains of HIV and one RNA transcript from two different viral strains are encapsidated into the same virion particle. This virion then infects a new cell where it undergoes replication. During this phase, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes. This recombination is most obvious when it occurs between subtypes.

Three groups of HIV-1 have been identified on the basis of differences in env: M, N and O [38](Figure 7). Group M is the most prevalent and is subdivided into eight subtypes, based on the whole genome, that are each geographically distinct [39]. The most prevalent are subtypes B (found predominantly in North America and Europe), A and D (found predominantly in Africa), and C (found predominantly in Africa and Asia) (Figure 8); these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1 (Figure 7). Coinfection with distinct subtypes gives rise to circulating recombinant forms (CRFs).

The first CRFs to be isolated were the AG recombinant from west and central Africa, the AGI recombinant from Cyprus and Greece, the AB recombinant from Russia, and the AE virus from Southeast Asia. However, the parent subtype E of CRF01_AE has not yet been identified and its status as a recombinant is in dispute.

In 2000, the last year in which an analysis of global subtype prevalence was made, 47.2% of infections worldwide were of subtype C, 26.7% were of subtype A/CRF02_AG, 12.3% were of subtype B, 5.3% were of subtype D, 3.2% were of CRF_AE, and the remaining 5.3% were composed of other subtypes and CRFs [40] (Figure 8). Almost 95% of all HIV research currently taking place is focused on subtype B, while a few laboratories focus on other subtypes.


Treatment
HIV infection is a chronic infectious disease that can be treated, but not yet cured. There are effective means of preventing complications and delaying, but not preventing, progression to AIDS. At the present time, not all persons infected with HIV have progressed to AIDS, but it is generally believed that the majority will. People with HIV infection need to receive education about the disease and treatment so that they can be active partners in decision making with their health care provider.

A combination of several antiretroviral agents, termed Highly Active Anti-Retroviral Therapy HAART, has been highly effective in reducing the number of HIV particles in the blood stream (as measured by a blood test called the viral load). This can improve T-cell counts. This is not a cure for HIV, and people on HAART with suppressed levels of HIV can still transmit the virus to others through sex or sharing of needles. There is good evidence that if the levels of HIV remain suppressed and the CD4 count remains greater than 200, then life and quality of life can be significantly prolonged and improved.

Treatment guidelines are constantly changing. The current guidelines for antiretroviral therapy (ART) from the World Health Organization reflect the 2003 changes to the guidelines and recommend that in resource-limited settings, HIV-infected adults and adolescents should start ART when HIV infection has been confirmed and one of the following conditions is present[41]:

Clinically advanced HIV disease:
WHO Stage IV HIV disease, irrespective of the CD4 cell count;
WHO Stage III disease with consideration of using CD4 cell counts <350/µl to assist decision making.
WHO Stage I or II HIV disease with CD4 cell counts <200/µl
The treatment guidelines in the USA are set by the United States Department of Health and Human Services (DHHS). The current guidelines for adults and adolescents were stated on April 7, 2005[42]:

All patients with history of an AIDS-defining illness or severe symptoms of HIV infection regardless of CD4+ T cell count receive ART.
Antiretroviral therapy is also recommended for asymptomatic patients with <200 CD4+ T cells/µl
Asymptomatic patients with CD4+ T cell counts of 201–350 cells/µl should be offered treatment.
For asymptomatic patients with CD4+ T cell of >350 cells/µl and plasma HIV RNA >100,000 copies/ml most experienced clinicians defer therapy but some clinicians may consider initiating treatment.
Therapy should be deferred for patients with CD4+ T cell counts of >350 cells/µl and plasma HIV RNA <100,000 copies/mL.
Because HIV disease progression in children is more rapid than in adults, and laboratory parameters are less predictive of risk for disease progression, particularly for young infants, treatment recommendations from the DHHS have been more aggressive in children than in adults [43].

There are several concerns about antiretroviral regimens. The drugs can have serious side effects. Regimens can be complicated, requiring patients to take several pills at various times during the day. If patients miss doses, drug resistance can develop [44].

As yet, no vaccine has been developed to prevent HIV infection or disease in in people who are not yet infected with HIV, but the potential worldwide public health benefits of such a preventive vaccine are vast. Researchers in many countries are seeking to produce such a vaccine, including through the International aids vaccine initiative.

In 2005, the Centers for Disease Control and Prevention in the United States recommended a 28-day HIV drug regimen for those who have been exposed to HIV (HIV Postexposure Prophylaxis [PEP] [45]). The drugs have demonstrated effectiveness in preventing the virus nearly 100% of the time in those who received treatment within the initial 24 hours of exposure. The effectiveness falls to 52% of the time in those who are treated within 72 hours; those not treated within the first 72 hours are not recommended candidates for the regimen.


Transmission and Epidemiology

Figure 9. The adult HIV prevalence at the end of 2004
HIV is transmitted through penetrative and oral sex whether vaginal or anal, blood transfusion, the sharing of contaminated needles through drug injection and in health care settings, and between mother and infant during pregnancy, childbirth and breastfeeding [46]. The use of physical barriers such as the latex condom is widely advocated to reduce the sexual transmission of HIV. Recently, it has been proposed that male circumcision may reduce the risk of HIV transmission [47], but many experts believe that it is premature to recommend male circumcision as part of HIV prevention programs [48].

At the end of 2004 there were between 36 and 44 million people living with HIV, of whom 25 million were in sub-Saharan Africa. Global estimates for new HIV infection in 2004 were 4.3-6.4 million. [49].

The epidemic is not homogeneous within regions with some countries more afflicted than others (Figure 9). Even at the country level there are wide variations in infection levels between different areas. The number of people living with HIV continues to rise in all parts of the world, despite strenuous prevention strategies.


Sub-Saharan Africa
Sub-Saharan Africa remains the hardest-hit region. HIV infection is becoming endemic in sub-Saharan Africa. It is home to just over 10% of the world’s population but more than 60% of all people living with HIV worldwide reside here. The adult (15-49) HIV prevalence rate is 7.4% (range: 6.9-8.3%). However, it must be noted that the actual prevalence does vary between regions. Across Sub-Saharan Africa, more women are infected with HIV than men, with 13 women living with HIV for every 10 infected men and the gap continues to grow. Throughout the region, women are being infected with HIV at earlier ages than men. The differences in infection levels between women and men are most pronounced among young people (aged 15–24 years). In this age group, there are 36 women living with HIV for every 10 men. The widespread prevalence of sexually transmitted diseases, the practice of scarification, transfusion, and the poor state of hygiene and nutrition in Africa may all be facilitating factors in the transmission of HIV-1 in this region ([50]. In 2000, the World Health Organization estimated that 25% of the units of blood transfused in Africa were not tested for HIV, and that 5-10% of HIV infections in Africa were transmitted via blood [51].


North Africa and the Middle East
The prevalence in this area is just 0.3%, with just 540,000 people infected. In this area, the routes of transmission of HIV is diverse, including paid sex, sex between men and injecting drug use. Among young people 15–24 years of age, 0.3% of women [0.1–0.8%] and 0.1% of men [0.1–0.3%] were living with HIV by the end of 2004.


South and South-East Asia
The HIV prevalence rate across this region is very small (0.6%). However, due to the population size, a higher total of HIV infections (7,100,000 adults and children) and annual AIDS deaths (490,000) occur in this region than any other region except sub-Saharan Africa. This sprawling region is not just vast but diverse, with the nature, pace and severity of HIV epidemics differing across the region. However, the AIDS picture in South Asia remains dominated by the epidemic in India. Latest estimates show that about 5.1 million people are currently infected with HIV in this country. In Asia, the HIV epidemic remains largely concentrated in injecting drug users, men who have sex with men, sex workers, and clients of sex workers and their immediate sexual partners. Effective prevention strategies in these populations are, for the most part, inadequate.


East Asia
Compared with other continents, notably Africa, the national HIV prevalence levels in Asia are low (0.1% in the adult (15-49) group). However, due to the large populations of many Asian nations, this low national HIV prevalence still means that large numbers of people are living with HIV. The picture in this region is dominated by China, with HIV prevalent in all regions of China. Much of the current spread of HIV in China is through injecting drug use and paid sex. In Japan, HIV transmission is mainly among men who have sex with men, some of whom might also be transmitting the virus to female sex partners.


Eastern Europe and Central Asia
An epidemic of HIV is currently occurring in Eastern Europe and Central Asia, with the number of people living with HIV rising dramtically. There are now an estimated 1.4 million people currently living with HIV in this region, though the adult (15-49) prevalence rate is low (0.8%). Injecting drug use is the main driving force behind epidemics across this region. The epidemic is still in its early stages in this region, which means that prevention strategies may be able to halt and reverse this epidemic. However, transmission of HIV is increasing through sexual contact and drug use among the young (<30 years). Indeed, over 80% of current infections occur in this region in people less than 30 years of age.


Western Europe
In this area, the routes of transmission of HIV is diverse, including paid sex, sex between men, injecting drug use, mother to child and heterosexual sex. However, many new infections in this region occur through contact with HIV-infected indivduals from other regions. The adult (15-49) prevalence in this region is 0.3% with 570,000 people currently living with HIV. Due to the availability of antiretroviral therapy, AIDS deaths have stayed low since the lows of the late 1990s. However, in some countries, a large share of HIV infections remain undiagnosed and there is worrying evidence of antiretroviral drug resistance among some newly HIV-infected individuals in this region. Also, there has been a recent increase in risky behaviour among men who have sex with men.


North America
The adult prevalence rate in this region is 0.6% with 1 million people currently living with HIV. The majority of people currently living with HIV in the USA are men who have sex with men. AIDS is one of the top three causes of death for African American men aged 25–54 and for African American women aged 35–44 years in the United States of America. It is possible that the high incarceration rates for African American men, could play an important factor in the epidemic through injecting drug use and unprotected sex in prison institutions. The main route of transmission for women is through heterosexual sex, and the main risk factor here is non-protection and the undisclosed risky behaviour by their sexual partners.


Caribbean
The Caribbean is the second-most affected region in the world. Among adults aged 15–44, AIDS has become the leading cause of death. The adult prevalence rate is 2.3%. HIV transmission occurrs largely through heterosexual intercourse, with two thirds of AIDS cases in this region attributed to this route. Sex between men is also a significant route of transmission, even though it is heavily stigmatised and illegal in many areas. HIV transmission through injecting drug use remains rare, except in Bermuda and Puerto Rico.


Latin America
In this region, only Guatemala and Honduras have national HIV prevalence of over 1%. In these countries, HIV-infected men outnumber HIV-infected women by roughly 3:1. Lower prevalence in other countries disguises serious, localized epidemics. Brazil accounts for more than a third of all HIV infections in Latin America, with the routes of transmission including paid sex, sex between men and injecting drug use.


Oceania
There is a very large range of national situations reagrding AIDS and HIV in this region. This is due, in part, to the large distances between the islands of Oceania. The wide range of development in the region also plays an important role. The prevalence is 0.2%, with 35,000 adults and children currently living with HIV.


References
^ Barré-Sinoussi, F., Chermann, J. C., Rey, F., Nugeyre, M. T., Chamaret, S., Gruest, J., Dauguet, C., Axler-Blin, C., Vezinet-Brun, F., Rouzioux, C., Rozenbaum, W. and Montagnier, L. (1983) Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS) Science 220, 868-871 PMID 6189183
^ Bentwich, Z., Kalinkovich., A. and Weisman, Z. (1995) Immune activation is a dominant factor in the pathogenesis of African AIDS. Immunol. Today 16, 187-191 PMID 7734046
^ Bukrinsky M, Adzhubei A. (1999) Viral protein R of HIV-1. Rev Med Virol 9, 39-49 PMID 10371671
^ Campbell GR, Pasquier E, Watkins J, Bourgarel-Rey V, Peyrot V, Esquieu D, Barbier P, de Mareuil J, Braguer D, Kaleebu P, Yirrell DL, Loret EP. (2004) The glutamine-rich region of the HIV-1 Tat protein is involved in T-cell apoptosis. J. Biol. Chem. 279, 48197-48204 PMID 15331610
^ Campbell GR, Watkins JD, Esquieu D, Pasquier E, Loret EP and Spector SA (2005) The C-terminus of HIV-1 Tat modulates the extent of CD178 mediated apoptosis of T cells. J. Biol. Chem. In Press. PMID 16155003
^ Carr, J. K., Foley, B. T., Leitner, T., Salminen, M., Korber, B. and McCutchan, F. (1998) Reference Sequences Representing the Principal Genetic Diversity of HIV-1 in the Pandemic. In: Los Alamos National Laboratory (Ed) HIV Sequence Compendium, pp. 10-19
^ Chan, D. C. and Kim, P. S. (1998) HIV entry and its inhibition. Cell 93, 681-684 PMID 9630213
^ Clerici, M., Balotta, C., Meroni, L., Ferrario, E., Riva, C., Trabattoni, D., Ridolfo, A., Villa, M., Shearer, G.M., Moroni, M. and Galli, M. (1996) Type 1 cytokine production and low prevalence of viral isolation correlate with long-term non progression in HIV infection. AIDS Res. Hum. Retroviruses. 12, 1053-1060 PMID 8827221
^ Coakley, E., Petropoulos, C. J. and Whitcomb, J. M. (2005) Assessing chemokine co-receptor usage in HIV. Curr Opin Infect Dis. 18, 9-15. PMID 15647694
^ Coffin, J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich, N., Temin, H., Toyoshima, K., Varmus, H., Vogt, P. and Weiss, R. A. (1986) What to call the AIDS virus? Nature 321, 10. PMID 3010128.
^ DHHS (2005) Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents April 7, 2005
^ DHHS (2005) Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection March 24, 2005
^ Dybul, M., Fauci, A. S., Bartlett, J. G., Kaplan, J. E., Pau, A. K., and the Panel on Clinical Practices for Treatment of HIV. (2002) Guidelines for using antiretroviral agents among HIV-infected adults and adolescents. Ann Intern Med 137, 381-433 PMID 12617573.
^ Gao, F., Bailes, E., Robertson, D. L., Chen, Y., Rodenburg, C. M., Michael, S. F., Cummins, L. B., Arthur, L. O., Peeters, M., Shaw, G. M., Sharp, P. M. and Hahn, B. H. (1999) Origin of HIV-1 in the chimpanzee Pantroglodytes troglodytes. Nature 397, 436-441 PMID 9989410
^ Gelderblom, H. R. (1997) Fine structure of HIV and SIV. In: Los Alamos National Laboratory (Ed) HIV Sequence Compendium, 31-44.
^ Gendelman, H. E., Phelps, W., Feigenbaum, L., Ostrove, J. M., Adachi, A., Howley, P. M., Khoury, G., Ginsberg, H. S. and Martin, M. A. (1986) Transactivation of the human immunodeficiency virus long terminal repeat sequences by DNA viruses. Proc. Natl. Acad. Sci. U. S. A. 83, 9759-9763 PMID 2432602
^ ICTVdB Descriptions. 61.0.6. Lentiviruses.
^ ICTVdB Descriptions. 61. Retroviridae.
^ Jeang, K. T. (1996) In: Human Retroviruses and AIDS: A Compilation and Analysis of Nucleic Acid and Amino Acid Sequences. Los Alamos National Laboratory (Ed.) pp. III-3–III-18
^ Kahn, J. O. and Walker, B. D. (1998) Acute Human Immunodeficiency Virus type 1 infection. N Engl J Med 331, 33-39 PMID 9647878.
^ Kim JB, Sharp PA. (2001) Positive transcription elongation factor B phosphorylates hSPT5 and RNA polymerase II carboxyl-terminal domain independently of cyclin-dependent kinase-activating kinase. J. Biol. Chem. 276, 12317-12323 PMID 11145967
^ Knight, S. C., Macatonia, S. E. and Patterson, S. (1990) HIV I infection of dendritic cells. Int Rev Immunol. 6,163-75 PMID 2152500
^ Learmont JC, Geczy AF, Mills J, Ashton LJ, Raynes-Greenow CH, Garsia RJ, Dyer WB, McIntyre L, Oelrichs RB, Rhodes DI, Deacon NJ, Sullivan JS. (1999) Immunologic and virologic status after 14 to 18 years of infection with an attenuated strain of HIV-1. A report from the Sydney Blood Bank Cohort. N Engl J Med 340, 1715-1722 PMID 10352163
^ Lévy, J. A. (1993) HIV pathogenesis and long-term survival. AIDS 7, 1401-1410 PMID 8280406
^ Morgan, D., Mahe, C., Mayanja, B. and Whitworth, J. A. (2002a) Progression to symptomatic disease in people infected with HIV-1 in rural Uganda: prospective cohort study. BMJ 324, 193-196 PMID 11809639
^ Morgan, D., Mahe, C., Mayanja, B., Okongo, J. M., Lubega, R. and Whitworth, J. A. (2002b) HIV-1 infection in rural Africa: is there a difference in median time to AIDS and survival compared with that in industrialized countries? AIDS 16, 597-6032 PMID 11873003
^ MMWR weekly (2005) Antiretroviral Postexposure Prophylaxis After Sexual, Injection-Drug Use, or Other Nonoccupational Exposure to HIV in the United States January 21, 54 (RR02), 1-20
^ Osmanov, S., Pattou, C., Walker, N., Schwardlander, B., Esparza, J. and the WHO-UNAIDS Network for HIV Isolation and Characterization. (2002) Estimated global distribution and regional spread of HIV-1 genetic subtypes in the year 2000. J. Acquir. Immune. Defic. Syndr. 29, 184-190 PMID 11832690
^ Piatak, M., Jr, Saag, M. S., Yang, L. C., Clark, S. J., Kappes, J. C., Luk, K. C., Hahn, B. H., Shaw, G. M. and Lifson, J.D. (1993) High levels of HIV-1 in plasma during all stages of infection determined by competitive PCR. Science 259, 1749-1754 PMID 8096089
^ Pollard, V. W. and Malim, M. H. (1998) The HIV-1 Rev protein. Annu Rev Microbiol. 52, 491-532 PMID 9891806
^ Popovic, M., Sarngadharan, M. G., Read, E. and Gallo, R. C. (1984) Detection, isolation, and continuous production of cytopathic retroviruses (HTLV-III) from patients with AIDS and pre-AIDS. Science 224, 497-500 PMID 6200935
^ Quiñones-Mateu, M. E., Mas, A., Lain de Lera, T., Soriano, V., Alcamí, J., Lederman, M. M. and Domingo, E. (1998) LTR and tat variability of HIV-1 isolates from patients with divergent rates of disease progression. Virus Research 57, 11-20 PMID 9833881
^ Reeves, J. D. and Doms, R. W. (2002) Human immunodeficiency virus type 2. J. Gen. Virol. 83, 1253-1265 PMID 12029140
^ Siegfried N, Muller M, Deeks J, Volmink J, Egger M, Low N, Walker S, Williamson P. (2005) HIV and male circumcision--a systematic review with assessment of the quality of studies. Lancet Infect Dis 5, 165-173 PMID 15766651
^ Strebel, K (2003) Virus-host interactions: role of HIV proteins Vif, Tat, and Rev. AIDS 17 Suppl 4, S25-S34 PMID 15080177
^ Tang, J. and Kaslow, R. A. (2003) The impact of host genetics on HIV infection and disease progression in the era of highly active antiretroviral therapy. AIDS 17, S51-S60 PMID 15080180
^ Thomson, M. M., Perez-Alvarez, L. and Najera, R. (2002) Molecular epidemiology of HIV-1 genetic forms and its significance for vaccine development and therapy. Lancet Infect Dis. 2, 461-71 PMID 12150845
^ UNAIDS How can HIV be transmitted]
^ UNAIDS (2004) AIDS epidemic update December 2004
^ Xiao, H., Neuveut, C., Tiffany, H. L., Benkirane, M., Rich, E. A., Murphy, P. M. and Jeang, K. T. (2000) Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1. Proc. Natl. Acad. Sci. U. S. A. 97, 11466-11471 PMID 11027346
^ WHO (2001) WHO/AFRO Press Release from the 51st Session of the WHO regional committee for Africa.
^ WHO (2003) Scaling up retroviral therapy in resource limited settings
^ WHO (2005) 26 July WHO/UNAIDS statement on South African trial findings regarding male circumcision and HIV
^ Wyatt, R. and Sodroski, J. (1998) The HIV-1 envelope glycoproteins: fusogens, antigens, and immunogens. Science 280, 1884-1888 PMID 9632381
^ Zheng, Y. H., Lovsin, N. and Peterlin, B. M. (2005) Newly identified host factors modulate HIV replication. Immunol Lett. 97, 225-234 PMID 15752562

See also
Criminal Transmission of HIV
HIV positive people
HIV test
List of HIV-positive people
Post-exposure prophylaxis
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