NICOTINE PATCH TO REDUCE POST SURGICAL PAIN

The use of a nicotine patch successfully used to help many smokers decrease their dependency on nicotine was shown to reduce pain in men after prostate removal surgery in a new anesthesiology study.

While morphine and other opioids (narcotics) remain the most commonly prescribed post-operative pain medications, many patients fear the side effects from these drugs, which can include drowsiness, nausea, slowed breathing, vomiting, constipation, itching and dependence.

Dr. Habib's study included 90 non-smoking men about to undergo a radical retropubic prostatectomy. Each received a 7-milligram nicotine patch or an identical placebo patch before anesthesia and surgery. After surgery, each patient was able to access morphine through a self-controlled device.

The patients who received the nicotine patch self-administered significantly less morphine in the postoperative period. In general, the nicotine patch was well-tolerated by patients, however, patients receiving nicotine reported higher levels of nausea.

Several previous studies have shown the pain-relief benefits of nicotine. In one study, a small dose of nicotine (3 milligrams) was given post-surgically, via a nicotine spray, to hysterectomy patients. These patients reported less pain and less need for morphine.

Future studies could determine whether nicotine is better administered in a patch or spray form, Dr. Habib said, as well as the effectiveness of nicotine in "smokers versus non-smokers and women versus men."

'SEED' THERAPY FOR BREAST TUMOUR REMOVAL

Physicians at UT Southwestern Medical Center are the first in Texas to use a new technique in which a small radioactive pellet, or "seed", is implanted into a mass or suspicious lesion in the breast to pinpoint its exact location for surgical removal.

During the procedure, a radiologist uses a needle to insert a small radioactive seed, about the size of a grain of rice, into the mass. Once lodged, surgeons use a wand that detects radioactivity to locate the mass and find the best pathway for removal.

"The new technique is less invasive for the patient and allows us to be more precise when removing possible breast-cancer tumors," said Dr. Roshni Rao, a surgical oncologist who specializes in breast cancer.
Previously, a radiologist would lance a thin, hooked wire into the breast to help guide the surgeon to the location of the mass. While one end of the wire was lodged at or near the mass, the other end protruded from the patient's skin.

Often, Dr. Rao said, the entry site of the wire was distant from the ideal site where a surgeon would prefer to make an incision. The wire also did not always take a direct path to the lesion.

The seed procedure pinpoints the location of a nonpalpable tumor more accurately than the wire and it is more efficient, Dr. Rao said. The wire method, on the other hand, requires patients to undergo the pre-operative procedure just hours before surgery because if left in longer, the wire could become dislodged.

"With the seed technique, the patient can have the seed inserted up to five days before surgery, any time of day," Dr. Ulissey said. "The seed procedure also increases efficiency in the radiology department since we are not locked into a two-hour window to insert the wire on the day of the surgery."

GENETIC MAKE-UP AFFECTS MULTIPLE SCLEROSIS

Magnetic resonance images (MRI) of a large group of patients with multiple sclerosis has provided the first evidence that those with a history of MS in their families show more severe brain damage than patients who have no close relatives with the disease.

The results, based on brain MRIs of 759 consecutive MS patients, support the hypothesis that a patient's genetic make-up plays a role not only in development but also in severity of the disease.

A University at Buffalo team of neurologists and imaging experts headed by Robert Zivadinov, M.D., Ph.D., professor of neurology, conducted the research


MS destroys myelin, the fatty sheath that protects nerve fibers carrying message traffic from various muscles to and from the central nervous system. For reasons currently unknown, in some people the myelin sheath breaks down, resulting in destruction of the nerve fibers and the symptoms of MS.

This demyelization process leads to mild to serious disability, from slight numbness of the limbs to loss of vision and paralysis.

The cohort of 759 patients involved in the study ranged in age from 36-56, with an average disability score of 3.4 on a scale of 0-10. A higher number indicates more disability.

Of these patients, 478 had relapsing-remitting MS, involving acute attacks with full or partial recovery; 222 had secondary-progressive MS, characterized by occasional attacks and sustained progression; 30 had primary-progressive MS with steady worsening from onset, and 29 had experienced their first attack.

Twenty-six percent, or 198, had a positive family history of MS. The breakdown between first-, second- or third-degree relatives with MS was 81/35/82. All patients obtained full clinical and quantitative MRI evaluations.

Using MRI, researchers measured the number and volume of lesions (plaques), which represent areas of demeylination; atrophy of the whole brain, white matter (the neural pathways), grey matter (brain regions) and the cortex, as well as employing additional imaging techniques.

There were no significant differences between familial and sporadic cases based on age, disease duration, disease course, disability score and total lifetime use of disease-modifying drugs.

Analysis showed that compared to patients with no family history of MS, familial MS patients had significantly more destructed lesions, and significantly lower volume of whole brain, white matter and gray matter, as well as other indications of greater brain degradation.

"Patients whose parents, children or siblings [first-degree relatives] had MS showed more damage than patients who had cousins with MS," Zivadinov said. "This indicates that the closer the relationship, the greater the risk of MS.

"Of particular interest is the finding of more severe gray matter damage and more lesions, particularly in those with MS in first-degree relatives. These findings are very interesting and we will be investigating them further."

BLOOD TEST TO PREDICT ALZHEIMER'S DISEASE

One of the most distressing aspects of Alzheimer's disease is the difficulty in determining whether mild memory problems are the beginning of an inevitable mental decline. Researchers at the Stanford University School of Medicine have developed a blood test that is a step toward giving people an answer two to six years in advance of the onset of the disease.

The test identifies changes in a handful of proteins in blood plasma that cells use to convey messages to one another. The research team discovered a connection between shifts in the cells' dialog and the changes in the brain accompanying Alzheimer's. They found that the blood test could indicate who had Alzheimer's with 90 percent agreement with clinical diagnoses, and could predict the onset of Alzheimer's two to six years before symptoms appeared.


Currently, the clinical diagnosis for Alzheimer's is one of exclusion -- by testing for other causes of memory loss and cognitive declines, such as stroke, tumors and alcoholism. If those conditions are eliminated as causes of memory loss, what remains is Alzheimer's, which is the most common cause of dementia. Even the clinical diagnosis is imperfect, and the only definitive diagnosis is by brain autopsy after a person has died.

NEW HIV FIGHITING DRUG GOT FDA APPROVAL

The Food and Drug Administration on Friday approved the first of a new class of HIV drugs that attacks the virus in a different way.

Isentress, developed by Merck & Co., is designed for patients who have shown resistance to current treatments.

The drug has been approved for adults who already have been receiving treatment, but more testing is necessary before it is approved for new HIV patients or children, the company said in a statement.

Isentress belongs to a class of drugs called integrase inhibitors. These drugs work by blocking the integrase enzyme, which helps HIV replicate by inserting its DNA into new cells. Isentress is the first drug in the class to win FDA approval.

Dr. Anthony Fauci, a noted HIV expert and director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, said the FDA's approval "will be most welcome in the community of physicians taking care of HIV-infected patients."

"Its mechanism of action is particularly important in that it blocks the ability of the virus to integrate itself into the genes of cells," Fauci said. "This property of the virus to integrate is important in establishing the reservoir of virus in the body that has made it extremely difficult to eradicate HIV, even with prolonged treatment."

Two earlier classes of anti-HIV drugs -- protease and reverse transcriptase inhibitors -- also work by blocking different enzymes involved in HIV replication. Friday's decision by the FDA will give doctors a new tool to help patients who have developed resistance to existing drugs or who are infected with drug-resistant strains of HIV.

Like protease and reverse transcriptase inhibitors, Isentress will also be prescribed for patients in combination with other drugs to maximize the number of ways the virus is being attacked.

The cost of the recommended daily regimen of Isentress -- a 400 mg tablet taken twice a day -- will be comparable to protease inhibitors, with a wholesale price of $27, Merck said

NANO DIAMONDS TO REVOLUTIONIZE DRUG DELIVERY SYSTEM

Researchers at the Northwestern University have shown that nanodiamonds, not unlike a 14-karat diamond, are very efficient in delivering chemotherapy drugs to cells without the harmful effects that are usually associated with current drug delivery agents.
Their study, published online by the journal Nano Letters, is the first to demonstrate the use of nanodiamonds, a new class of nanomaterials, in biomedicine. In addition to delivering cancer drugs, the model could be used for other applications, such as fighting tuberculosis or viral infections, say the researchers.

Nanodiamonds promise to play a significant role in improving cancer treatment by limiting uncontrolled exposure of toxic drugs to the body. The research team reports that aggregated clusters of nanodiamonds were shown to be ideal for carrying a chemotherapy drug and shielding it from normal cells so as not to kill them, releasing the drug slowly only after it reached its cellular target.

Another advantage of the material, confirmed by a series of genetic studies also reported in the paper, is that nanodiamonds do not cause cell inflammation once the drug has been released and only bare diamonds are left. Materials currently used for drug delivery can cause inflammation, a serious complication that can predispose a patient to cancer, block the activity of cancer drugs and even promote tumor growth.

“There are a lot of materials that can deliver drugs well, but we need to look at what happens after drug delivery,” said Dean Ho, assistant professor of biomedical engineering and mechanical engineering at Northwestern’s McCormick School of Engineering and Applied science who led the research. “How do cells react to an artificial material left in the body? Nanodiamonds are highly ordered structures, which cells like. If they didn’t, cells would become inflamed. From a patient’s perspective, this is very important. And that’s why clinicians are interested in our work.”

NON RESPONCE TO ANTI-DEPRESSANTS AFTER MI PREDICTS FUTURE CARDIAC EVENTS

Among patients with myocardial infarction (MI) who subsequently develop depression, a lack of response to antidepressants signals a high risk of future cardiac events, according to a subanalysis of data from Myocardial Infarction and Depression-Intervention Trial (MIND-IT)

MIND-IT involved 2,177 patients hospitalized with an acute MI. During follow-up, 375 patients developed post-MI depression, with 209 patients randomized to mirtazapine 30 mg/day, or "care as usual." If there was an inadequate response to mirtazapine after 8 weeks, open treatment with citalopram was allowed in the intervention group.

Dr. Peter de Jonge of the University Medical Center Groningen, the Netherlands, and colleagues report in the American Journal of Psychiatry for September that the recurrent cardiac event rate was 25.6% among nonresponders, 11.2% among untreated control subjects and 7.4% among responders.

After adjustment for potential cofounders, nonresponders had a hazard ratio of 2.92 for new cardiovascular events in comparison to untreated controls.

"This study provides further preliminary evidence that nonresponse to treatment of post-myocardial infarction depression may be associated with cardiac events," the investigators conclude.

"Our present findings leave the possibility open that post-myocardial depression may be causally involved in cardiovascular prognosis," Dr. de Jonge and colleagues add. "However, the actual test for causality has to wait until the long-term course of post-myocardial infarction depression can be altered by more effective treatment

CHIKUNGUNYA FEVER

INTRODUCTION:Chikungunya fever is a mosquito-borne viral disease with symptoms such as fever, joint pain, muscle pain, headache and nose and gum bleeding.

Chikungunya is endemic in parts of Africa, Southeast Asia and on the Indian sub-continent. In the summer of 2007 an outbreak of chikungunya started in the province of Ravenna in the Emilia-Romagna region of North-Eastern Italy. At the moment Ravenna is considered to be an area where transmission of chikungunya is taking place.

Infectious agent: The Chikungunya virus is an arbovirus (alphavirus of the family of Togaviridae); this is a heat-sensitive RNA virus. The virus was first isolated in Tanzania and Uganda in 1953. The name origins from the posture of the patients: in Makonde language, chikungunya means: « that which bends up ».

Reservoir: The main virus reservoirs are monkeys, but other species can also be affected, including humans.

Transmission modes: In urban areas (where most of the outbreaks have been reported in Asia), the disease is transmitted from human to human by Aedes mosquitoes (Aedes aegypti, albopictus, polynesiensis). In La Réunion, where a large outbreak occurred in 2005-2006, the vecor was Aedes albopictus, a daytime vector with highest activity at the beginning and end of the day. This is also the suspected vector in the current Italian outbreak. Among monkeys, the disease is transmitted by Aedes furcifer and africanus.

Clinical presentation : Incubation ranges from 1 to 12 days, with an average of 4 to 7 days. The main clinical symptoms in patients are fever, joint pain, muscle pain and headache. Benign haemorrhagic symptoms, such as bleeding from the nose or gums, are possible, in particular in children. While most of the cases recover without consequences, the development of a more chronic phase is possible, with persistent joint pains. Recovery may take several weeks for these patients, coinciding with pronounced lethargy. During the outbreak in La Réunion, severe complications have been described, including respiratory failure, cardio-vascular decompensation, or meningo-encephalitis.

Epidemiology :Chikungunya is endemic in parts of Africa, Southeast Asia and on the Indian sub-continent. In Africa, cases have been described between 1957 and 1974 in Transvaal, Uganda, Congo, Nigeria, Ghana, and South Rhodesia (now Zimbabwe). Serologic studies have also shown the virus in Senegal, Burkina Faso, the Central African Republic, Cameroon, and Guinea-Bissau. More recently, the virus was documented in Asia, in particular in the Philippines, Malaysia, Cambodia, southern India and Pakistan. In 2005-06, a major outbreak affected several islands in the Indian Ocean, moving from the Comoro Islands, to other islands in the Indian Ocean, Mauritius, Mayotte, Madagascar, Seychelles and La Réunion, an overseas department of France. In La Réunion, a total of 266 000 cases were reported, with 254 deaths, mostly occurring in elderly patients with an underlying medical condition. In 2006, other countries reporting outbreaks of chikungunya included India, Sri Lanka, The Maldives, Malaysia and Indonesia. During this period, imported cases of chikungunya among tourists were reported in several European countries.

Areas of Chikungunya virus transmission in 2007: In 2007, apart from an outbreak in Gabon in the beginning of the year, and cases reported from Indonesia and Madagascar, the majority of the chikungunya cases were mostly being reported from India. As from August 2007, an outbreak is reported in the province of Ravenna in the Emilia-Romagna region in Italy with local mosquito-borne transmission. If the local transmission is confirmed, it is the first time that Chikungunya virus is known to be transmitted by mosquitoes within Europe.

Treatment: Symptomatic only (non-steroid anti-inflammatories, non-salicylic analgetics).

Information to visitors to areas of transmission: pregnant women, immuno-deprived people and people suffering from a severe chronic illness should consult their physicians prior to the travel in order to assess their risk and get recommendations on personal preventive measures.
All travellers to the countries where chikungunya fever is occurring should take the following preventive measures to minimise the exposure to mosquito bites while in the areas:

1. Use of anti-mosquito devices (insecticide-treated bed nets, spray, repellents) and wearing long sleeve – long leg clothes, especially during the hours of highest mosquito activity.
2. Mosquito repellent based on a 30% DEET concentration is recommended. Before using repellents, pregnant women and children under the age of 12 years should consult a physician or pharmacist. For newborn children under three months, repellents are not recommended; instead, insecticide-treated bed nets and protective clothing should be used.
3. Pregnant women, immuno-deprived people and people suffering from a severe chronic illness should consult their physicians prior to the travel in order to assess their risk and get recommendations on personal preventive measures.

Other preventive measures: Measures at the community level include

1. Reduction of mosquito breeding sites (removal of all open containers with stagnant water in and round houses, or, if that is not possible, treatment with larvicides)
2. In affected areas, elimination of adult mosquitoes through aerial spraying with insecticides

AIDS

What are the early symptoms of HIV infection?

Many people do not develop any symptoms when they first become infected with HIV. Some people, however, get a flu-like illness within three to six weeks after exposure to the virus. This illness, called Acute HIV Syndrome, may include fever, headache, tiredness, nausea, diarrhoea and enlarged lymph nodes (organs of the immune system that can be felt in the neck, armpits and groin). These symptoms usually disappear within a week to a month and are often mistaken for another viral infection.

During this period, the quantity of the virus in the body will be high and it spreads to different parts, particularly the lymphoid tissue. At this stage, the infected person is more likely to pass on the infection to others. The viral quantity then drops as the body's immune system launches an orchestrated fight.

More persistent or severe symptoms may not surface for several years, even a decade or more, after HIV first enters the body in adults, or within two years in children born with the virus. This period of "asymptomatic" infection varies from individual to individual. Some people may begin to have symptoms as soon as a few months, while others may be symptom-free for more than 10 years. However, during the "asymptomatic" period, the virus will be actively multiplying, infecting, and killing cells of the immune system.

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What Happens Inside the Body?

Once HIV enters the human body, it attaches itself to a White Blood Cell (WBC) called CD4. Also, called T4 cells, they are the main disease fighters of the body. Whenever there is an infection, CD4 cells lead the infection-fighting army of the body to protect it from falling sick. Damage of these cells, hence can affect a person's disease-fighting capability and general health.

After making a foothold on the CD4 cell, the virus injects its RNA into the cell. The RNA then gets attached to the DNA of the host cell and thus becomes part of the cell's genetic material. It is a virtual takeover of the cell. Using the cell's division mechanism, the virus now replicates and churns out hundreds of thousands of its own copies. These cells then enter the blood stream, get attached to other CD4 cells and continue replicating. As a result, the number of the virus in the blood rises and that of the CD4 cells declines.

Because of this process, immediately after infection, the viral load of an infected individual will be very high and the number of CD4, low. But, after a while, the body's immune system responds vigorously by producing more and more CD4 cells to fight the virus. Much of the virus gets removed from the blood. To fight the fast-replicating virus, as many as a billion CD4 cells are produced every day, but the virus too increases on a similar scale. The battle between the virus and the CD4 cells continues even as the infected person remains symptom-free.

But after a few years, which can last up to a decade or even more, when the number of the virus in the body rises to very high levels, the body's immune mechanism finds it difficult to carry on with the battle. The balance shifts in favour of the virus and the person becomes more susceptible to various infections. These infections are called Opportunistic Infections because they swarm the body using the opportunity of its low immunity. At this stage, the number of CD4 cells per millilitre of blood (called CD4 Count), which ranges between 500 to 1,500 in a healthy individual, falls below 200. The Viral Load, the quantity of the virus in the blood, will be very high at this stage.

Opportunistic infections are caused by bacteria, virus, fungi and parasites. Some of the common opportunistic infections that affect HIV positive persons are: Mycobacterium avium complex (MAC), Tuberculosis (TB), Salmonellosis, Bacillary Angiomatosis (all caused by bacteria); Cytomegalovirus (CMV), Viral hepatitis, Herpes, Human papillomavirus (HPV), Progressive multifocal leukoencephalopathy (PML) (caused by virus); Candidiasis, Cryptococcal meningitis (caused by fungus) and Pneumocystis Carinii pneumonia (PCP). Toxoplasmosis. Cryptosporidiosis (caused by parasites). HIV positive persons are also prone to cancers like Kaposi's sarcoma and lymphoma.

The Center for Disease Control (CDC), Atlanta has listed a series of diseases as AIDS-defining. When these diseases appear, it is a sign that the infected individual has entered the later stage of HIV infection and has started developing AIDS. The progression of HIV positive persons into the AIDS stage is highly individual. Some people can reach the AIDS stage in about five years, while some remain disease free for more than a decade. Measurement of the viral load and the CD4 count helps a doctor in assessing an infected person's health condition.

What are the later symptoms of HIV/AIDS?

Lack of energy Weight loss Frequent fevers and sweats A thick, whitish coating of the tongue or mouth (thrush) that is caused by a yeast infection and sometimes accompanied by a sore throat Severe or recurring vaginal yeast infections Chronic pelvic inflammatory disease or severe and frequent infections like herpes zoster Periods of extreme and unexplained fatigue that may be combined with headaches, lightheadedness, and/or dizziness Rapid loss of more than 10 pounds of weight that is not due to increased physical exercise or dieting Bruising more easily than normal Long-lasting bouts of diarrhoea Swelling or hardening of glands located in the throat, armpit, or groin Periods of continued, deep, dry coughing Increasing shortness of breath The appearance of discoloured or purplish growths on the skin or inside the mouth Unexplained bleeding from growths on the skin, from mucous membranes, or from any opening in the body Recurring or unusual skin rashes Severe numbness or pain in the hands or feet, the loss of muscle control and reflex, paralysis or loss of muscular strength An altered state of consciousness, personality change, or mental deterioration Children may grow slowly or fall sick frequently. HIV positive persons are also found to be more vulnerable to some cancers.

IS THERE ANY TREATMENT? Till today, there is no conclusive treatment to eliminate HIV from the body; however, timely treatment of opportunistic infections can keep one healthy for many years. The commonly available treatment for AIDS is the treatment against opportunistic infections. Normally standard treatment regimens, used against such infections in non-HIV patients, also work well with the HIV-positive persons. If properly treated, almost all the opportunistic infections can be contained. However, during the last decade, researchers have developed powerful drugs that check the replication of the virus at various levels. Called Antiretroviral drugs, they are available in three classes and under various brands. Taken in combinations (called cocktail or combination therapy) under specialised medical advice, these drugs drastically reduce the viral load in blood. However, they do not permanently cure one of HIV. This line of treatment, called HAART (Highly Active Antiretroviral Therapy) has resulted in a huge reduction or AIDS-related deaths. Though many positive persons and caregivers have welcomed these drugs, others have experienced serious side effects. They are also very expensive and are out of reach for a majority of the infected people. But of late, the prices have been steeply falling. The three classes of drugs are: Nucleoside analogue Reverse Transcriptase Inhibitors (NRTIs). NRTIs were the first antiretroviral drugs to be developed. They inhibit the replication of HIV in the early stage by inhibiting an enzyme (which is necessary for viral replication) called Reverse Transcriptase. The drugs include Zidovudine (Retrovir, AZT), Lamivudine (Epivir, 3TC), Didanosine (Videx, ddI), Zalcitabine (Hivid, ddC), Stavudine (Zerit, d4T) and Abacavir (Ziagen). The major reported side effect of Zidovudine is bone marrow suppression, which causes a decrease in the number of red and white blood cells. The drugs ddI, ddC and d4T can damage peripheral nerves (peripheral neuropathy), leading to tingling and burning in the hands and feet. Treatment with ddI can also cause pancreatitis, and ddC may cause mouth ulcers. Approximately 5 percent of people treated with Abacavir experience hypersensitivity reactions such as a rash along with fever, fatigue, nausea, vomiting, diarrhea and abdominal pain. Hypersensitivity reactions can also occur without a rash. In either case, symptoms usually appear within the first 6 weeks of treatment and generally disappear when the drug is discontinued. If a person had a hypersensitivity reaction to Abacavir, he/she should avoid taking the drug again. Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs). These drugs bind directly to the enzyme, Reverse Transcriptase. There are three NNRTIs currently approved for clinical use: Nevirapine (Viramune), Delavirdine (Rescriptor) and Efavirenz (Sustiva). A major side effect of all NNRTIS is a rash. In addition, people taking Efavirenz may have side effects such as abnormal dreams, sleeplessness, dizziness and difficulty concentrating. Protease inhibitors (PIs). PIs interrupt HIV replication at a later stage in its life cycle by interfering with an enzyme known as HIV protease. This causes HIV particles in the body to become structurally disorganized and noninfectious. Among these drugs are Saquinavir (Fortovase), Ritonavir (Norvir), Indinavir (Crixivan), Nelfinavir (Viracept), Amprenavir (Agenerase) and Lopinavir (Kaletra). The most common side effects of PIs include nausea, diarrhoea and other digestive tract problems. They can also cause a significant number of side effects when they interact with certain other medications. That is because all PIs, to one degree or another, affect an enzyme system in the liver that is responsible for metabolising a large number of drugs. Newer side effects have also appeared with the continuing and widespread use of Protease Inhibitors. These include elevated triglyceride levels and problems with sugar metabolism that may sometimes progress to diabetes. There may also be abnormalities in the way fat is metabolised and deposited in the body. Some people lose much of their total body fat while others gain excess fat on the back between their shoulders (buffalo hump) or in the stomach (protease paunch). Right now, no one knows exactly why these abnormalities occur. In fact, it is not even certain whether these problems are a direct result of treatment with protease inhibitors or due to some other cause that has yet to be identified. Similar metabolic abnormalities have occurred in people on antiretroviral therapy that does not include PIs. Although these body changes can be distressing, the possibility they may occur should not stop one from obtaining treatment for HIV/AIDS. In simple combination therapy, some physicians prescribe a combination of RTIs. But in HAART, which in fact has made a dramatic change in AIDS treatment, a combination of RTIs and PIs is prescribed. People respond differently to treatment and maintaining the drug schedule is extremely important. Indiscriminate treatment results in drug resistance and resurgence of the viral load. Therefore it should be taken only under expert medical advice. What about vaccines? More than a dozen HIV vaccines are currently being tested. As of now, there is no vaccine to prevent HIV infection. What is Parent to Child Transmission? Babies born to mothers infected with HIV may or may not be infected with the virus, but all carry their mothers' antibodies to HIV for several months after birth. If these babies lack symptoms, a definitive diagnosis of HIV infection using standard antibody tests cannot be made until after 15 months of age. By then, the babies are unlikely to still carry their mothers' antibodies and will have produced their own, if they are infected. New technologies to detect HIV itself are being used to more accurately determine HIV infection in infants between ages 3 months and 15 months. A number of blood tests are being evaluated to determine if they can diagnose HIV infection in babies younger than 3 months.

AIDS No other word engenders as much fear, revulsion, despair and utter helplessness as AIDS. Despite increased AIDS awareness, the terror persists. AIDS is, in fact, rewriting medical history as humankind's deadliest scourge. With 40 million deaths forecast in this millennium, statistics tell their own sordid tale. The first recorded sample of HIV was discovered in 1959 in a blood specimen obtained at Leopoldville (now Kinshasa) in the Belgian Congo. This was the first known death chalked up by AIDS. The HIV is thought to have originally affected chimpanzees. The crossover of the virus from animals to humans may have occurred in the 1950s through an accident or a bite. Intermittently, other theories of its origins have been advanced during the ongoing process of AIDS research. One theory, put forward by Bette Korber, traces the disease to a single viral ancestor that could have emerged between 1910 and 1950. Through an AIDS research analysis done at the Los Alamos National Lab in New Mexico, Korber contends that the pandemic may have come from one or more infected humans around 1930. Another highly controversial—but plausible—theory is that of American philosopher, Louis Pascal, first spelt out in 1987. All the early AIDS cases originated in the Central African states of Congo, Rwanda or Burundi. This belt was subjected to trials of a live polio vaccine on 300,000 men, women and children. Pascal argued that the vaccine, which was grown in cultures obtained from chopped up chimpanzee kidneys, may have carried this virus. Polio researcher Dr Albert Sabin had reported that such a batch was contaminated by an unknown virus. In fact, monkeys harbor SIV or simian immunodeficiency virus (SV-40 to be more specific), which is thought to be the ancestor of HIV. The first cases of AIDS were reported in the United States in 1981, amongst male homosexuals in Los Angeles and New York. Within two decades, up to 50 million may have been infected globally, approximately 22 million have succumbed and nearly 15,000 new infections are said to occur daily. With a definite AIDS cure still in the research stages, an increased AIDS awareness, counseling and alternative therapy treatments seem to offer the only succor. HIV has two major categories: HIV-1 and HIV-2. HIV-1, which currently has about 10 subtypes, is most common worldwide and the only form found in the US. HIV-2 is less virulent and though currently confined to West Africa—it's spreading. The Human Immunodeficiency Virus (HIV) basically provokes an infection, which destroys the body's immune system. And AIDS or Acquired Immune Deficiency Syndrome is the advanced stage of this disease, when the immune system becomes irreparably damaged, engendering multiple infections and cancers. A person is considered HIV positive when s/he tests positive for any of the 26 diseases (Kaposi's sarcoma, lymphoma, pulmonary tuberculosis, recurrent pneumonia within a 12-month period, wasting syndrome and other indicators) that can easily invade the body during our immune system's nonfunctionality. On invading the body, the virus specifically attacks T-cells. A core part of the human defence system, they mobilize other cells to seek and destroy contagious foreign elements besid es leading the immune system's fight against infections. T-cells are targeted because the AIDS virus parasitizes the CD4 molecules on their surface. With a protective outer shell of proteins and glyco-proteins, the AIDS virus contains genetic information on the inside. Although substantially smaller than the host T-cells—the virus reproduces by sponging off the host's cellular resources! Our body fights back by producing up to two billion new T-cells to replace the infected ones, stabilizing the T-cell count temporarily. Yet from day one, the T-cells fight a losing battle. The genetic information of the AIDS virus, which is encoded as RNA (ribonucleic acid), needs to be reverse transcripted—which the intruder accomplishes with the help of the host cell itself! The now legible DNA is thereafter randomly transferred into the nucleus. All this is accomplished barely a dozen hours following the infection. By this time, the aggressor begins to substantially weaken the host cell, which eventually dies, eroding the immune system and making the body vulnerable to diseases. Although HIV targets T-cells and other cells in the body, it thrives mainly in the lymph nodes—another important part of the immune system. Each lymph node has a netlike structure inside it that acts as a protective filter by trapping virus and infected T-cells. But as healthy T-cells move through contaminated lymph nodes, they are infected by HIV. Particularly during the early stage of the disease, lymph nodes contain more infected cells than the blood.

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In the early stages, a mild flu and swollen glands are typical. But the symptoms are often unmistakeable when full-blown AIDS develops. Loss of appetite, weight loss, constant fever, prolonged fatigue, diarrhea, constipation, changing bowel patterns, swollen glands, chills coupled with excessive sweating, especially at nights, lesions in the mouth, sore throat, persistent cough, shortness of breath, tumours, skin rashes, headaches, memory lapses, swelling in the joints, pain in various parts of the body, vision problems and a regular feeling of lethargy and ill health make up the litany of symptoms. With immune systems out of kilter, HIV-positive persons are susceptible to several types of cancer, particularly Kaposi's sarcoma (KS), an uncommon form that occurs under the skin and in the mucus membranes of the eyes, nose and mouth. Affected persons have lesions that appear as dark-coloured raised blotches. Though the lesions are painless, once KS spreads to the lungs, lymph nodes and digestive tract, the victim experiences difficulty in breathing, gastrointestinal bleeding and painful swelling around the lymph nodes, especially in the legs.

HIV is transmitted primarily by sex (anal, vaginal or oral sex with an infected partner), by injections (sharing contaminated needles for drug use or accidental piercing with a contaminated needle), or from infected mother to child through pregnancy or breast-feeding. Infected semen and vaginal fluids, infected blood and blood products lead to the transmission of HIV. Drug abuse with unsterilized needles is another high-risk activity. Unprotected sex with multiple partners is the primary cause of infection. During unprotected sex, the infected fluid could enter the bloodstream through a tiny cut or a sore. Anal penetration has a higher risk of transmission, which is why a high percentage of homosexuals develop the disease. Bleeding during sex also raises the chances of infection. Therefore unprotected sex during menstrual periods and anal intercourse are best avoided. An infected mother can also transmit the virus to her baby before or during birth or through breast milk. Although traces of HIV have been detected in body fluids (saliva, urine, faeces and tears) there is no evidence that HIV spreads through these fluids. Nor is it water-borne, air-borne or transmitted through mosquitoes and other insects. Some HIV-infected patients progress to AIDS quickly while others can remain healthy for 10 years or more. Between initial infection and full-blown disease, a middle phase called symptomatic HIV infection, or AIDS-related complex (ARC), occurs, prompting symptoms such as weight loss, diarrhea, and swollen lymph glands. Scientists have recently discovered clues to why some patients develop AIDS quickly. In a study published last March in the journal Science, National Cancer Institute researchers found that inherited genes may set the clock for AIDS progression. Certain gene patterns tend to stave off AIDS, while others promote it. The researchers say the study may help lead to an AIDS-preventive vaccine or improved therapies against the virus.

Gender Differences in the Risk of HIV Infection HIV risk factors among injection drug users (IDUs) differ markedly by gender, according to a 10-year study funded by the National Institute on Drug Abuse (NIDA). A recent study by researchers at the Johns Hopkins University reported that while drug-related risk behaviors and homosexual activity are the most important predictors of HIV seroconversion among males, factors consistent with high-risk heterosexual activities are the main predictors among females. The findings, reported in the May 28 (2001) issue of the Archives of Internal Medicine, provide insight into the relationship between gender and high-risk sexual behaviors in the development of HIV infection. "Early studies of injection drug users suggested that most HIV infections were due primarily to sharing needles," said NIDA Director Alan I. Leshner, Ph.D. "This study adds to the body of evidence that supports the need for gender-specific interventions in the treatment of that group of drug users." Between 1988 and 1998, a team of researchers, led by Dr. Steffanie Strathdee at the Johns Hopkins University Bloomberg School of Public Health, examined both drug related and sexual risk factors for HIV transmission in a study of more than 1,800 injecting drug users in Baltimore, Maryland. Study participants were aged 18 or older, did not have an AIDS defining illness at enrollment, and reported a history of illicit injection drug use within the previous 10 years. Through semiannual interviews, researchers collected data on drug use history, sociodemographics, and drug use and sexual behavior within the last 6 months. Blood samples were also obtained at each study visit. Researchers used commercial HIV and antibody ELISA to identify those participants who had become HIV positive since their last visit. Dr. Strathdee and her colleagues found that the greatest predictor for HIV seroconversion among both male and female IDUs was high-risk sexual behavior. Study findings revealed that male injection drug users who reported recent homosexual activity were four times more likely to become infected with HIV. Among females, indicators of high-risk heterosexual activity outweighed needle-sharing behaviors as independent predictors of HIV seroconversion. HIV incidence was more than two times higher among women who reported recently having sex with another injection drug user. Another common predictor of HIV seroconversion observed by researchers among both male and female IDUs was younger age. Investigators found that IDUs who were aged 30 or younger at enrollment were more than twice as likely to seroconvert than those aged 40 or older. "This is consistent with several reports which indicate that younger IDUs are more likely to engage in needle sharing and other behaviors that place them at higher risk of acquiring HIV and hepatitis B or C viruses," stated Dr. Strathdee.

Say 'AIDS' and dime-a-dozen misconceptions abound. The chart topper is that AIDS is supposedly a disease of gay men and intravenous drug users. The facts are otherwise. No doubt in the early years many HIV-positive cases were reported amongst the Western gay community. In recent years, however, prevalence rates among gays have leveled off. Instead, heterosexual transmission has been forging ahead of all other modes of transmission. The AIDS virus is NOT contracted through touching, hugging, kissing, massage, sharing toilet seats, drinking or eating from utensils used by an infected person or any other mode of casual contact. Nor does working, socialising and living with infected people cause the disease. Repeated sexual contact without proper precautions with an infected person, using an infected syringe, exposure to infected blood or sexual fluids are ways through which the disease can be transmitted. Donating blood also does not run the risk of disease contraction since needles used for such purposes are always sterile. Since the AIDS virus is unable to survive outside the human body beyond a short duration, dried blood is not infectious For this reason, mosquitoes are incapable of transmitting HIV as the virus cannot replicate itself in the intestine of insects. Although medical personnel are potentially at risk from infection, this is minimal if protective gear such as gloves, masks and goggles are always used when handling potentially infected material.

The Elusive Cure The large-scale infections and deaths have spurred a spate of worldwide efforts for a cure. In the US, however, AIDS cases are said to be dropping and new infections leveling off. Mortality from AIDS is also dropping. In the developing countries, though, the cases continue to rise alarmingly. Globally, three million died in the year 2000, with 5.3 million newly infected people, 95 percent of whom might die. Many scientists, doctors and researchers contend that AIDS is not a new disease, having been around much longer than people believe. Dr. Robert Willner—author of Deadly Deception: The Proof That Sex and HIV Absolutely Do Not Cause AIDS—asserts that HIV is not the cause of AIDS. He claims that nearly 500 hundred top scientists of the world have challenged the hypothesis of Robert Gallo—who patented the HIV test the day after the AIDS virus was discovered—that HIV is the precursor of AIDS. Besides other telling facts, the dissenters want to know how one can explain HIV-free AIDS cases, of which there are said to be nearly 5,000 on record. Dr. Frank Shallenberger, a licensed medical and homeopathic practitioner, says that statistics are only a correlation—not a result—that HIV is one cause of AIDS, citing the fact that some AIDS victims do not have HIV antibodies. Dr. Shallenberger considers AIDS a multifactorial disease that strikes when the immune system is down. The search for a cure, also brings to light other interesting facets. African chimpanzees have been harboring the simian equivalent of the AIDS virus for centuries, according to detailed studies conducted by researches at the University of Alabama in Birmingham. Why don't the chimps succumb to the virus? Says Dr. Anthony Fauci from the National Institutes of Health: "There must be something about the chimp's immune system or some host defense system that is doing a very good job of containing the virus. If we find that out we may be able to extrapolate to humans." Chimpanzees being the closest living relatives of humans, their DNA differs from human DNA by less than two percent. Adds Dr. Fauci: "It's entirely conceivable that the very small genetic differences between the chimp and the human will explain why the chimpanzee does not get sick and the human does."