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AIDSInfo-at-a-glance

Issue No. 28 | July 09, 2010
A Service of the U.S. Department of Health and Human ServicesView HTML version
News and Features 

NIH-Led Scientists Find Antibodies that Prevent Most HIV Strains from Infecting Human Cells

“Scientists have discovered two potent human antibodies that can stop more than 90 percent of known global HIV strains from infecting human cells in the laboratory, and have demonstrated how one of these disease-fighting proteins accomplishes this feat. According to the scientists, these antibodies could be used to design improved HIV vaccines, or could be further developed to prevent or treat HIV infection. Moreover, the method used to find these antibodies could be applied to isolate therapeutic antibodies for other infectious diseases as well. ...

“Led by a team from the NIAID Vaccine Research Center (VRC), the scientists found two naturally occurring, powerful antibodies called VRC01 and VRC02 in an HIV infected individual's blood ... using a novel molecular device they developed that homes in on the specific cells that make antibodies against HIV. The device is an HIV protein that the scientists modified so it would react only with antibodies specific to the site where the virus binds to cells it infects.

“The scientists found that VRC01 and VRC02 neutralize more HIV strains with greater overall strength than previously known antibodies to the virus.

"The researchers also determined the atomic-level structure of VRC01 when it is attaching to HIV.  This has enabled the team to define how the antibody works and to precisely locate where it attaches to the virus. With this knowledge, they have begun to design components of a candidate vaccine that could teach the human immune system to make antibodies similar to VRC01 that might prevent infection by the vast majority of HIV strains worldwide.”

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Summer 2010 Issue of mental health AIDS is Released

The quarterly biopsychosocial research update on HIV and mental health, mental health AIDS, is sponsored by the Center for Mental Health Services (CMHS) of the Substance Abuse and Mental Health Services Administration (SAMHSA) and is disseminated free of charge through the SAMHSA Web site in both PDF and HTML formats.

The Summer 2010 issue features "HIV & Hepatitis C: Coping with Coinfection (Part 2)."

Part 1 of this series provided a medical, psychiatric, psychosocial, and neuropsychological overview of HIV/hepatitis C virus (HCV) coinfection, the process of determining eligibility for HCV treatment, and the important role mental health clinicians play in assessing eligibility and intervening with clients who elect to receive treatment for HCV.

This concluding segment expands on how providers make the decision to offer HCV treatment to individuals living with HIV and chronic HCV infection, how coinfected individuals make decisions to accept or defer treatment for HCV, and the latest thinking on HCV treatment interventions.

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Study Suggests Gene Therapy Leads to HIV Resistance in Mice

“CCR5 is the major HIV-1 co-receptor, and individuals homozygous for a 32-bp deletion in CCR5 are resistant to infection by CCR5-tropic HIV-1. Using engineered zinc-finger nucleases (ZFNs), we disrupted CCR5 in human CD34(+) hematopoietic stem/progenitor cells (HSPCs) at a mean frequency of 17% of the total alleles in a population. This procedure produces both mono- and bi-allelically disrupted cells. ZFN-treated HSPCs retained the ability to engraft NOD/SCID/IL2rgamma(null) mice and gave rise to polyclonal multi-lineage progeny in which CCR5 was permanently disrupted. Control mice receiving untreated HSPCs and challenged with CCR5-tropic HIV-1 showed profound CD4(+) T-cell loss. In contrast, mice transplanted with ZFN-modified HSPCs underwent rapid selection for CCR5(-/-) cells, had significantly lower HIV-1 levels and preserved human cells throughout their tissues. The demonstration that a minority of CCR5(-/-) HSPCs can populate an infected animal with HIV-1-resistant, CCR5(-/-) progeny supports the use of ZFN-modified autologous hematopoietic stem cells as a clinical approach to treating HIV-1.”

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