New Treatment Allows Patient’s Immune System to Combat HIV

A study published in Cell Host & Microbe suggests that adding small molecules that imitate the T cell receptor CD4 to antiretroviral therapy could make latent HIV susceptible to the patient's own antibodies. The researchers are hopeful this could eventually lead to the elimination of long-term antiretroviral treatment as a necessity for patients with HIV.

Antiretroviral therapy, the most common treatment for HIV, works to halt the replication of the virus. However, the treatment then becomes a lifelong necessity for the patient, as they continue to harbor latent HIV in a small number of immune system cells. If the treatment is halted, the virus can again replicate and can potentially develop into AIDs.

To conduct the study, the investigators stopped antiretroviral treatment for mice carrying human plasma and blood cells infected with HIV. Then, they treated the mice with the CD4-like drug, which binds to and exposes vulnerable parts of the viral envelope on infected cells. According to the researchers, the mice experienced either no rebound of infection or long delays before active HIV infection restarted.

“These antibodies are like pawns,” said Priti Kumar, PhD, in a press release. “There are many of them, but they are useless against the source of virus. But with the right move, they can be promoted to a powerful position and score a decisive victory by eliminating infected cells.”

The CD4-like molecules act to expose the virus in infected cells, allowing the antibodies to recognize it and trigger an immune response. The antibodies then signal the patient’s natural killer cells, which act to rid the body of the infected cells.

“In this way, a patient's own antibodies and cells that are commonly present can eliminate the viral reservoir and prevent viral rebound," Kumar said in the release. "The hope is one day we might be able to do away with antiretroviral therapies altogether.”

REFERENCE

Molecule enlists patient's immune system to combat HIV [news release]. EurekAlert; May 20, 2021. Accessed May 25, 2021. https://eurekalert.org/pub_releases/2021-05/yu-mep051921.php