| AIDS pins at a conference in Toronto
New Delhi, Feb. 15: A quarter of a century after the human immunodeficiency virus-1 (HIV) was discovered, scientists have identified its very first target cells in the human vagina that allow it entry into the body.
Researchers at the University of Washington School of Medicine in Seattle have found that HIV-1 simultaneously enters two different types of cells of the immune system found within the inner cells of the vagina.
“Our findings shed light on the very earliest steps of mucosal HIV infection... and may guide the design of effective strategies to block local transmission and prevent HIV-1 spread,” researcher Juliana McElrath and her colleagues said.
They reported their findings in the journal Immunity.
Heterosexual contact is a major route through which HIV-1 has been spreading across the world. While scientists have been struggling to develop vaccines to protect people from HIV-1 infection, they have also been searching for ways to interfere with virus transmission by trying to understand the sequence of initial events in the infection.
The researchers developed a model to study the precise mechanisms through which HIV-1 enters the lower female reproductive tract.
They isolated cells from a lining called the epithelium and observed immune cells that usually move out of the vaginal epithelium into deeper tissues soon after exposure to HIV-1.
They found that HIV-1 enters two classes of immune cells — Langerhans cells (LC) and CD4+ T cells — but through different mechanisms.
Both LC and CD4+ cells move out of the vaginal epithelium after the infection.
The study has shown that the CD4+ cells may be primarily responsible for local shedding of the virus in the vagina of women infected with HIV-1, while LC may hold the virus for some time before spreading it to other cells.
While scientists have known for several years that HIV-1 enters CD4+ cells by interacting with a protein called CCR5, its route of entry into the LC appears to be more complex and diverse.
The scientists have pointed out that this has implications for the development of topical microbicides that are being designed to block the entry of HIV-1.
, a virus that was recognised as a distinct disease-causing microorganism in 1981."Our findings also underscore the need for a topical microbicide tointerfere with viral entry into LC as well, and this will not beachieved by blocking CCR5 alone," the researchers said in theirreport.