So far, viral load - the amount of virus in the blood of an HIV-infected person - has been viewed as the key indicator of a patient's progression to AIDS.
However, researchers led by Sunil Ahuja, M.D., of the University of Texas Health Science Center in San Antonio, the combination of two key genes involved in cell-mediated immunity may help predict the course of infection.
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According to scientists, variations in the CCR5 and CCL3L1 genes may affect immune system response to HIV and replication of the virus.
CCR5 controls a key receptor on the surface of the CD4 immune cell onto which HIV attaches, while CCL3L1 controls an immune system signaling molecule called a chemokine, which blocks HIV from attaching to the CCR5 receptor, the researchers said.
![AIDS - Progression]( "AIDS - Progression")
The disease progression varies widely among individuals depending on host susceptibility, genetics, immune function, health care, co infections and the viral genetic variability
For the study, the researchers examined genetic information from more than 3,500 HIV-1 infected and uninfected individuals. They found that individuals who had specific combinations of two genes—CCR5, which helps facilitate HIV entry into the cell, and CCL3L1, an immune response gene—were much more likely to have reduced immune responses and a greater decline in CD4 T cells, two hallmarks of progressive HIV disease.
Further, the researchers found that in HIV-infected subjects, viral load contributed only 9 percent to the variability in rate of progression to AIDS; variations in CCR5 and CCL3L1 combined accounted for 6 percent variability in AIDS progression rates.
'The genetic variations contribute nearly as much to the extent of inter-individual variability in AIDS progression rates as does HIV-1 viral load,' Nature quoted Ahuja, as saying.
He added that the findings may have implications for the care of HIV-infected individuals in terms of being able to more effectively predict the course of HIV disease.
Researchers say that other genes may also play a role but more research is required to determine that.
The study was funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
Source: ANI
SPH/C
AIDS - Progression
The disease progression varies widely among individuals depending on host susceptibility, genetics, immune function, health care, co infections and the viral genetic variability
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For the study, the researchers examined genetic information from more than 3,500 HIV-1 infected and uninfected individuals. They found that individuals who had specific combinations of two genes—CCR5, which helps facilitate HIV entry into the cell, and CCL3L1, an immune response gene—were much more likely to have reduced immune responses and a greater decline in CD4 T cells, two hallmarks of progressive HIV disease.
Further, the researchers found that in HIV-infected subjects, viral load contributed only 9 percent to the variability in rate of progression to AIDS; variations in CCR5 and CCL3L1 combined accounted for 6 percent variability in AIDS progression rates.
'The genetic variations contribute nearly as much to the extent of inter-individual variability in AIDS progression rates as does HIV-1 viral load,' Nature quoted Ahuja, as saying.
He added that the findings may have implications for the care of HIV-infected individuals in terms of being able to more effectively predict the course of HIV disease.
Researchers say that other genes may also play a role but more research is required to determine that.
The study was funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health.
Source: ANI
SPH/C
AIDS - Initial Theories and Disease Progression
AIDS was first detected in early 1980s, among gays, Haitians and black Africans. HIV is a descendant of a Simian Immunodeficiency Virus.
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Blood Test for AIDS/ HIV InfectionHow to confirm the presence of HIV in the patient through blood tests? Page also has international data of world population affected by HIV virus. | Advertisement
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