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Host protein p21 restricted HIV progression in elite controllers
The p21 host protein that inhibits HIV replication in hematopoietic stem cells appeared to restrict HIV infection in elite controllers. Manipulation of p21 may offer opportunities to increase hosts’ resistance to HIV infection, according to new findings presented by Mathias Lichterfeld, MD, PhD.
“This gene expression is much more strongly expressed in elite controllers,” Lichterfeld, instructor in medicine at Massachusetts General Hospital and Harvard Medical School, Boston, said during a press conference. “We do not fully understand why these certain patients have higher levels of the p21 protein, but this is something that is currently being investigated. If we were able to increase p21 expression in CD4 T cells in the broader population, we may then be able to increase resistance to HIV on a larger scale.”
Compared with CD4 T cells from all other patient cohorts, CD4 T cells from elite controllers were significantly less susceptible to HIV infection (P<.01). According to Lichterfeld, this resistance was due to less effective reverse transcription and HIV mRNA transcription from proviral DNA.
Moreover, defective viral replication in elite controllers led to a 10- to 20-fold increased expression of p21 in CD4 T cells from elite controllers (P<.001). Barriers of p21 significantly enhanced reverse transcription and HIV mRNA transcription in CD4 T cells in ex-vivo infection assay (P=.01).
“These data show the CD4 T cells in elite controllers are less susceptible to HIV infection when compared with other patients,” Lichterfeld said.
Lichterfeld. #819. Presented at: the IDSA 48th Annual Meeting; Oct. 21-24, 2010; Vancouver, B.C.