Linda Barlow

I’ve been following the swine flu scare quite closely, having long been interested in infectious diseases that have spread widely, causing the great pandemics of history.  One of the reasons I went back to grad school recently to study biology was because of my concern over the devastation wrought by HIV-AIDS.  I wanted to know more about these deadly agents that can cause so much misery and death.

Influenza subtype A H1N1 is frightening because, according to the CDC, it represents a novel mix of elements from human, bird, and pig influenza virus genomes.  When human immune systems are exposed to a new infectious agent, we have no existing antibodies to attack and neutralize it.  Thus, when confronted with such a pathogen, we’re more likely to get sick than if we had already had full or partial immunity.

Immunology is a highly complex discipline, however, and viruses are tricksy creatures.  From what I’ve been able to understand about the current situation, we’re still in the learning phase when it comes to A H1N1.  We just don’t know enough about it yet.  And even if we did, viruses evolve rapidly.  They lack some of the sophisticated error checkers that do quality control on replication in more complex eukaryotic cells (i.e., the kind of cells we humans are made of).  Thus viruses mutate quickly, which can result in increased or decreased lethality, transmission, and resistance to antiviral medications like Tamiflu.

Flu bugs tend to spread less in the warmer months, which is why our typical flu seasons start in the fall and end in the spring.  In the northern hemisphere, summer is approaching, which should lead to a drop-off of A H1N1 cases (although countries in the southern hemisphere might suffer an increase).  But the World Health Organization and the CDC are concerned that a summer drop-off might be the lull before the storm.  During the post-World War I influenza pandemic of 1918-19, which is believed to have killed 20-40 million people, the flu started in the spring, died down during the summer, then came back roaring the following fall/winter, killing far more efficiently than the usual flu virus.

From what I can make out from reading and digesting a lot of the current information that’s out there, the current H1N1 bug is nowhere near as scary as the 1918 version.  It’s not as lethal, it’s probably less contagious, and it’s apparently not causing death by cytokine storm (where you’re effectively destroyed by your own hyperactive immune reaction).  But viruses being somewhat unpredictable, this could change…which is why we’re being warned to stay alert, cover our mouths when we cough or sneeze, stay home from school/work if we’re sick, and wash our hands frequently with soap and warm/hot water.

This afternoon’s latest alert from the World Health Organization begins like this: “4 May 2009 — As of 18:00 GMT, 4 May 2009, 21 countries have officially reported 1085 cases of influenza A (H1N1) infection. Mexico has reported 590 laboratory confirmed human cases of infection, including 25 deaths. The United States has reported 286 laboratory confirmed human cases, including one death.”

Map of H1N1 cases

This week’s medical news brought a report about the disappointing results of one of the (thought to be) most promising weapons in the small arsenal against HIV-AIDS: a vaginal gel microbiocide, Carroguard. The gel was being tested in a large-scale trial in South Africa and Botswanna. This clinical trial had been ongoing for three years, but unfortunately, the number of women who became infected with HIV during the trial from the group who used Carroguard was very similar to the number of women in the control group who also seroconverted. Essentially, this means the drug did not work.

Granted, there are some questions about the results since it is always difficult to calculate whether the women in the study used the drug regularly and correctly. Did they faithfully insert the gel before having sex? If not, the results of the study may not reveal the entire picture.

Why is this news significant? There are currently about 33 million people infected with HIV-AIDS. Over the years, we have heard of many failures in the various HIV-AIDS agents and therapies, although there have also been some major successes. But the drugs that have been shown to fight the stubborn and infinitely clever HIV virus have not, thus far, prevented infection. Instead, therapies like Zidovudine (AZT) and Nevirapine (which prevent the HIV virus from replicating inside infected human cells) and the HIV protease inhibitors (which stop mature new viruses from being produced) interfere with the HIV virus’s activity after it has already infected its victim. Such agents, usually used in combination with each other, have given life and hope to millions of people infected with the HIV virus. But they do not cure AIDS, nor do they prevent the virus from entering human cells and beginning its deadly siege of the human immune system.

The microbiocide gels work in an entirely different manner. The goal for this type of drug is to prevent the transmission of the virus by blocking its initial entry into human cells. The point here is not to cure the disease, but to prevent a person being infected in the first place.

According to a 2004 report of the Joint UN/World Health Organization, a microbiocide, even if only 60 % effective, could result in a major reduction of new HIV infections among women. If applied vaginally prior to intercourse by 20 percent of women in 73 low income countries, it could prevent 2.5 million new infections over a three year period.

This assumes, of course, that the microbiocide works. Different microbiocides use different methods to achieve their goals – for more on this topic see WHO’s website.

Such an approach is urgently needed. During sexual intercourse, the receptive partner is more susceptible to the virus than the penetrative partner, meaning that women are more likely to acquire the virus from men than vice versa. Since power dynamics in relationships often make it difficult for women to insist upon the use of condoms, the development of a topical agent that women could apply prior to intercourse is vital.

There has generally been a failure by public health officials to recognize that gender inequality all too often deprives women of the right either to decline sex or to insist upon the use of condoms. This situation is worse in some countries than in others, and is related not only to the status of women in a particular nation, but also to their age, level of education, and personal power within their sexual relationships.

If effective microbiocides can be researched and developed, and if women can be taught to use them regularly, they could potentially prevent millions of new infections in the years to come. This would greatly benefit women at risk for AIDS, an important goal since women now represent 50 percent of the global total of AIDS-infected individuals. It would also benefit children, since it is believed that 97 percent of infants with AIDS acquire the virus from their mothers.

More info on microbiocides

Paper written by Linda Barlow on macrobiocides