One of the reasons HIV is so difficult to contain and treat is its rapid evolution. Understanding how host defenses and viral countermeasures contribute to that evolution is vital.
Host cells produce two proteins that mutate HIV DNA and interfere with the virus's ability to replicate. But HIV produces a protein, called Vif, that can disable the two defensive proteins.
Vif is full of variation, both in sequence and in function, according to a new study in PLoS Pathogens, and this could in turn potentially accelerate the evolution of HIV.
Within a single patient, some versions of Vif don't work at all; others counteract only one of the host's defensive proteins. "It's a leaky system," according to Paul D. Bieniasz, senior author of the study and associate professor at The Rockefeller University's Aaron Diamond AIDS Research Center.
Some variations in Vif only partially inactivate the defensive proteins that cause HIV to mutate, and might even promote further variation in the virus within patients. "This work elucidates new pathways which shape the evolution of the virus," says Viviana Simon, lead author of the study.
Page: 1 Related biology news :1
Contact: Paul Ocampo
Public Library of Science
. Variation in 3 genes influences risk of age-related macular degeneration2
. Variation in CHEK2 gene may triple breast cancer risk3
. Variation in bitter-taste receptor gene increases risk for alcoholism4
. Variation in immune response gene causes age-related macular degeneration when triggered5
. Variation in womens X chromosomes may explain differences among individuals, between sexes6
. HIVs cellular kiss of death explains loss of uninfected T cells in AIDS7
. Reading ability protects brain from lead exposure8
. Greenlands ancient forests shed light on stability of ice sheet9
. Which came first: Primates ability to see colorful food or see colorful sex?10
. Autism-related proteins control nerve excitability, researchers find11
. Sleep deprivation affects airport baggage screeners ability to detect rare targets