While we know that an estimated 1.1 million Americans are living with human immunodeficiency virus (HIV) and that 6,465 people died from the disease in 2015, what remains unknown is the breadth of HIV patients that suffer from the virus’s neurological impairments. HIV infection causes immune activation of the central nervous system (CNS), and this prolonged activation can eventually lead to neurological damage in HIV patients. However, clues about the process that causes these conditions have remained a mystery until now.
In research conducted by Shelli Farhadian, a Yale infectious disease specialist in the Spudich lab, in collaboration with the Yale Center for Genome Analysis, scientists used single-cell RNA sequencing, a recently-developed genetic technology, to detect microglia-like immune cells in the cerebrospinal fluid of patients with suppressed HIV infection. Previously, microglia were thought to have been found only in the brain, so their wayward presence is a compelling hint at processes in the disease that have previously gone undetected.
“Part of the problem might be that once HIV enters the brain during acute infection, it causes damage that becomes symptomatically evident years later,” said Farhadian.
Because CNS cells are challenging to study, the presence of these microglia-like cells in cerebrospinal fluid in the context of this technology can shed light not only on the etiology behind neurological damage in patients with HIV but also diseases such as Parkinson’s and Alzheimer’s.
“By characterizing these cells in more detail and in a variety of disease conditions, we may learn more about how microglia and microglia-like cells function to protect or to contribute to diseases, including neurological impairment related to HIV infection,” said Farhadian.