By Ethan Covey
A new analysis supports prior reports that people with sickle cell disease (SCD) have lower rates of HIV infection, but follow-up cell studies did not reveal a mechanism to explain the reduced risk (PLoS One 2020;15[4]:e0218880. doi: 10.1371/journal.pone.0218880).

A number of epidemiological reports have suggested that people with SCD experience low rates of HIV infection compared with the general population. However, the mechanisms behind this reduced risk remain unclear.

To better understand the reduced risk, Shannon Kelly, MD, of Vitalant Research Institute in San Francisco, and her colleagues conducted a two-part investigation. First, they ran a new statistical analysis of data from The Transfusion Safety Study, which was conducted from 1985 to 1993. The transfusion study looked at people with conditions characterized by a low red blood cell count, including SCD. They found that those with SCD experienced lower rates of HIV infection, according to Dr. Kelly.

The Transfusion Safety Study, which was conducted from 1985 to 1993, was retrospectively reviewed. Next, the researchers conducted a lab study of immune system cells isolated from blood samples from HIV-negative patients with or without SCD. They hypothesized that a lower risk for HIV infection might be related to molecular characteristics of immune system cells known as CD4+ T cells.

The lab studies found that CD4+ T cells from people with SCD had lower levels of CCR5, a key protein involved in HIV infection. These cells also had lower levels of the protein CCR7 and higher levels of the protein CD4. However, further experiments showed that the cells were no less susceptible to HIV infection than the CD4+ T cells from people without SCD.

These findings lend further support to the idea that people with sickle cell disease are less likely to be infected with HIV. However, further research is needed to determine whether the molecular differences uncovered in this study are related to this lower risk, or whether other mechanisms are at play.