Electron micrograph of herpes simplex virusFLICKR, NIAIDResearchers have traditionally designed vaccines against herpes simplex virus type 2 (HSV-2) to elicit antibodies that targeted the viral surface protein called glycoprotein D (gD-2), which the virus uses to enter host cells. But by deleting gD-2 from the viral genome, William Jacobs of the Albert Einstein College of Medicine and his colleagues not only rendered the virus unable to infect cells, they were able to develop a vaccine that forced the murine immune system to produce antibodies that recognize different viral targets.
“We had a hunch that gD-2 might be masking other viral antigens, and that by removing this dominant protein we would expose those previously masked antigens to the immune system,” Jacobs said in astatement.
Using the gD-2–lacking virus to immunize mice, the researchers elicited complete protection against wild-type HSV-2, both when the animals were challenged intravaginally or through the skin. Importantly, the researchers, who published their results this week (March 10) in eLife, found no evidence of latent HSV-2 lingering in the vaccinated mice.
“A dominant protein like that is like a loud person in a room; other people speaking can’t be heard,” coauthor Betsy Herold, a pediatric infectious disease doctor at Einstein, told Science News, drawing the analogy to gD-2 and other viral antigens.
“Our findings challenge the existing dogma that says an effective herpes vaccine must stimulate neutralizing antibodies against gD-2,” Jacobs said in the statement. “It’s almost as if the virus evolved gD-2 specifically to hide the other antigens; gD-2 turns out to be a Trojan horse that misleads the immune system.”
TAKEN FROM- THE SCIENTIST
No comments:
Post a Comment