Tale of Two Intersecting Epidemics: Why We Need mRNA Vaccines in Africa, and For All Who Are Immunocompromised

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2021-08-19 08:30:03

The views and opinions expressed here are those of the authors and do not necessarily reflect the position of either Johns Hopkins University and Medicine or the University of Washington.

This title is one Larry used twenty years ago when talking about the intersection between the sexually transmitted infection genital herpes (HSV-2) and HIV. At the time, he was describing how HSV-2 increased the risk of HIV acquisition and HIV made the severity of HSV-2 worse, and how this relationship between the two conditions created an epidemiological synergy with concomitant additional misery for humankind. This title is applicable today about the intersecting pandemics of HIV and COVID-19.

Individuals living with HIV have a degree of immunosuppression that varies based on their therapy and disease course. If the disease course is well controlled and fully virologically suppressed on antiretroviral therapy, there is evidence to believe that these patients are at a normal risk of acquiring and controlling COVID-19, much like others in their families and communities. This analogy is partially accurate in that those living with HIV can, because of their medicines, have obesity, diabetes, and increased lung disease, which are all predispositions or comorbidities associated with severe COVID-19.

Importantly, there are subsets of persons living with HIV – including those who are immune deficient with low T cell counts, those with viremia due to drug resistant HIV viral strains, those not receiving or not taking antiretroviral therapy, and the many millions we know are living with undiagnosed HIV infection, including those recently infected. These persons are subject to acquire persistent, prolonged SARS-CoV-2 infection, akin to organ transplant recipients and severely immunosuppressed cancer patients. There are many causes of immunocompromise but in many countries HIV infection is among the most common. A recent case report by Karim et al. from South Africa, the country with the largest percent of the population living with HIV, described a case of HIV infection in a person who had very low CD4 counts due to resistant virus and a lack of compliance who developed COVID-19. Over a period of 200 days, this patient – who was ambulatory, living in the community, and without serious symptoms – shed SARS-CoV-2. They had mild illness early on, which is why they were observed, and because of HIV, follow-up care ensued. The investigators had samples from the patient, and they shed SARS-CoV-2 at high titers, showing the development of multi-mutational changes in the virus over time. These mutational changes essentially recapitulated the Beta variant, which has 9 to 11 different mutational changes than the original ancestral strain. This case illustrates why we are writing this blog to talk about how individual patients living with HIV and compromised immune systems who have this prolonged shedding pattern can result in the kind of mutational changes that lead to germination and spread of variants of concern in our communities.