Lessons learned from the HIV Pandemic can be applied to COVID-19

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From the multitude of lessons gained in the over three decades-long conundrums of HIV/AIDS, Belizean Policy Makers can adapt some of those to the COVID-19 pandemic. HIV/AIDS has left in its wake a knowledge infrastructure that we can now build upon.
United Nations Secretary-General Antonio Guterres has approved a new report from the Joint United Nations Programme on HIV/AIDS UNAIDS, which examines how the experience in tracking HIV can help inform and guide COVID-19 responses. Belize’s response to HIV/AIDS can also be utilized as guidance to COVID-19.
Belize’s National AIDS Commission was appointed by Cabinet and officially established in February 2000. The principal objective of the NAC is to coordinate, facilitate, and monitor the national response to HIV/AIDS as well as the National Strategic Plan. The Commission also has the shared responsibility for Advocacy, Resource Mobilization, the development of Policy and Legislation, and overall monitoring and Evaluation of all interventions and efforts.
Having catalysed an unprecedented global mobilization that has succeeded in reversing a pandemic, which has claimed over 33 million lives, the HIV response is a natural source of guidance for responding to the new pandemic of COVID-19. Lessons learned from the HIV response offers social guidance for fighting COVID-19 on building political commitment and galvanizing research innovations in service delivery.
William Haseltine, a former Harvard Medical School professor writes “We are now engaged in another deadly episode in the historic battle of man versus microbe. These battles have shaped the course of human evolution and history. We have seen the face of our adversary, in this case, a tiny virus.”
Like all viruses, coronaviruses are expert code crackers. SARS-CoV-2 has certainly cracked ours. Think of this virus as an intelligent biological machine continuously running DNA experiments to adapt to the ecological niche it inhabits. This virus has caused a pandemic in large part because it acted on two of our human vulnerabilities: our biological defences and our clustering and patterns of social behaviour.
But several lessons from the long battle with HIV, the human immunodeficiency virus that causes AIDS, suggest what may lie ahead. HIV/AIDS is one of the worst scourges’ humans have encountered. As a code cracker, HIV is an expert. By the end of 2019, the global death toll from this virus was roughly 33 million people. In all, 76 million people have been infected, and scientists estimate another 1.7 million people acquire the virus every year.
Yet we must appreciate what our scientific defences have accomplished. Of the nearly 38 million people currently living with HIV/AIDS, 25 million are receiving full antiretroviral treatments that prevent disease and suppress the virus so well they are unlikely to pass it along. Dr. William Haseltine would wager that another 25 million or more infections never happened, primarily in sub-Saharan Africa, because these treatments became available in most countries.
From fighting this epic war against AIDS, doctors, virologists, epidemiologists, and public health experts have learned crucial lessons that we can apply to the battle we are currently waging. For instance, we saw that vaccines are never a guarantee but that treatments can be our most important weapon. We discovered that human behavior plays a vital role in any disease-fighting effort and that we cannot overlook human nature. We have also seen how critical it is to build on knowledge and tools gained fighting earlier outbreaks.
Early observations of how HIV behaves in our bodies showed the road to a vaccine would be long and challenging. As the outbreak unfolded, we began tracking antibody levels and T cells (the white blood cells that wage war against invaders) in those infected. The high levels of both showed that patients were mounting incredibly active immune responses, more forceful than anything we had seen for any other disease. But even working at its highest capacity, the body’s immune system was never strong enough to clear out the HIV virus completely.
Unlike the hit-and-run poliovirus, which evokes long-term immunity after infection, HIV is a “catch it and keep it” virus—if you are infected, the pathogen stays in your body until it destroys the immune system, leaving you undefended against even mild infections. Moreover, HIV continually evolves—a shrewd opponent seeking ways to elude our immune responses. Although this does not mean a vaccine is impossible, it certainly meant developing one, especially when the virus hit in the 1980s, would not be easy. “Unfortunately, no one can predict with certainty that an AIDS vaccine can ever be made,” Dr. William Haseltine testified in 1988 to the U.S Presidential Commission on the HIV Epidemic. “That is not to say it is impossible to make such a vaccine, only that we are not certain of success.” More than 30 years later there still is no effective vaccine to prevent HIV infection.
From what we have seen of SARS-CoV-2, it interacts with our immune system in complex ways, resembling polio in some of its behavior and HIV in others. We know from nearly 60 years of observing coronaviruses that a body’s immune system can clear them. That seems to be generally the case for SARS-CoV-2 as well. But the cold-causing coronaviruses, just like HIV, also have their tricks. Infection from one of them never seems to confer immunity to reinfection or symptoms by the same strain of the virus—that is why the same cold viruses return each season. These coronaviruses are not hit-and-run virus-like polio or a catch-it-and-keep-it virus like HIV.
The path to a SARS-CoV-2 vaccine may be filled with obstacles. Whereas some people with COVID-19 make neutralizing antibodies that can clear the virus, not everybody does. Whether a vaccine will stimulate such antibodies in everyone is still unknown. Moreover, we do not know how long those antibodies can protect someone from infection.
We learned with HIV that attempts to prevent virus entry altogether do not work well—not for HIV and not for many other viruses, including influenza and even polio. Vaccines act more like fire alarms: rather than preventing fires from breaking out, they call the immune system for help once a fire has ignited.
The first set of HIV drugs were nucleic acid inhibitors, known as chain terminator drugs. They inserted an additional “chain-terminating” nucleotide as the virus copied its viral RNA into DNA, preventing the HIV chain of DNA from elongating.
By the 1990s, experts had gotten better at using combinations of drugs to control HIV infections soon after patients were exposed. The first drug, AZT, found an immediate application for health care workers who accidentally had a needlestick injury that infected them with contaminated blood. It was also used to reduce mother-to-child transmission. For example, prenatal treatments for mothers with AIDS at that time reduced the number of babies born infected by as much as two thirds. Today combination chemotherapy reduces mother-to-child transmission to undetectable levels.
The next set of drugs was protease inhibitors. The first was introduced in 1995 and was combined with other drugs in treating patients. These drugs inhibited the viral protease enzyme responsible for longer precursor proteins in the short active components of the virus. But there is a fundamental problem with these drugs, as well as those that inhibit viral polymerases, which help to create virus DNA. Our bodies also use proteases for normal functioning, and we need polymerases to replicate our nucleic acids. The same drugs that inhibit the viral proteins also inhibit our cells. The difference between a concentration in which the drug inhibits the virus target and a concentration in which it hurts the human proteins is called the therapeutic index. The therapeutic index gives you the window in which the drug will be effective against the virus without causing undue side effects. That window is rather narrow for all polymerase and protease inhibitors.
The gold standard for AIDS treatment now is called antiretroviral therapy—essentially patients take a cocktail of at least three different drugs that attack HIV in different ways. The strategy is based on earlier success scientists had in fighting cancer. Cancers developed resistance over time to single drugs, but combinations of drugs were effective in slowing, stopping, or killing the cancers. Scientists took that same lesson of combination chemotherapy to HIV. By the early 1990s, the first combination AIDS treatments were saving the lives of people infected with HIV. Today an infection is far from the death sentence it used to be—patients can now live almost unaffected by HIV, with a relatively minimal impact on life expectancy.
Scientists already know resistance to single drugs will bedevil COVID-19 treatments. Experts have seen resistance to single, anti-SARS-CoV-2 drugs develop rapidly in early lab studies. Just as with AIDS and cancer, we need a combination of medicines to treat this disease. The goal of the biotechnology and pharmaceutical industries now is to develop an array of highly potent and specific drugs, each of which targets a different function of the virus. Decades of research on HIV has shown the way and gives us confidence in our eventual success.
There is likewise a sexual dynamic to COVID-19 that often goes unmentioned. It is part of what is driving people out of their homes and into bars and parties. Anyone with a craving for a beer can quench their thirst in the safety of their own home, but the gratification comes less easily for other desires, especially when one is young, single, and living alone. Our public health strategies should not ignore this fact.
The same lessons we learned amid the HIV epidemic to help young people change their behaviors apply today to COVID-19: know your risk, know your partners, and take necessary precautions. Many young people operate under the false assumption that even if they become infected, they will not become severely ill. Not only is this belief untrue, but even people with asymptomatic infections can suffer serious, lasting damage. But the more people understand the risk—younger people especially—the greater likelihood they will take the steps necessary to protect themselves and others. We saw this happen with AIDS.
Our toolset for virus and pharmaceutical research has improved enormously in the past 36 years since HIV was discovered. What used to take us five or 10 years in the 1980s and 1990s in many cases now can be done in five or 10 months. Experts can rapidly identify and synthesize chemicals to predict which drugs will be effective. They can do cryoelectron microscopy to probe virus structures and simulate molecule-by-molecule interactions in a matter of weeks—something that used to take years. Scientists would have no hope of beating COVID-19 if it were not for the molecular biology gains made during earlier virus battles.