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When multiple HIV variants are transmitted, difference in the fitness of different HIV variants and/or selective pressures act very early in infection to select one or a few founder strains, leading to homogenization of HIV env sequences [37].
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One of the topics of relevance to be analyzed is the ability of heterologous prime-boost immunization protocols to induce specific T-cell immune responses capable of recognizing multiple HIV-1 variants.
The combined analysis of phylogeny, maximum and mean distances, and Poisson fitness suggested that transmission of multiple HIV-1C variants occurred in 4 (20% of resolved, or 16% of analyzed) cases, while transmission of a single viral variant occurred in 16 (80% of resolved, or 64% of analyzed) cases.
Thus, while novel vectors and heterologous prime-boost combinations are getting better at inducing higher frequencies of HIV-1-specific T cells, less attention has been paid to how these vaccines can elicit T cells capable of recognizing multiple HIV-1 variants.
Unfortunately, the emergence of HIV variants with multiple resistance gene mutations resulted in a high HIV load and low CD4+ T cell count.
In adults, while HIV infection is usually initiated by one or a few HIV variants, some individuals are infected with multiple HIV strains [32], [33], [34], [35], [36].
Deep sequencing affords multiple advantages over current sequencing techniques for the detection of minority HIV variants.
Evolution of drug-resistant HIV variants remains a major limitation for the long-term control of HIV-1 infection as wide resistance to multiple drug classes is associated with clinical deterioration and death [ 3].
Analysis of HIV populations in vivo shows that after long-term suppressive cART, genetically identical HIV variants emerge (3, 4).
In terms of HIV evolution, why is it more effective to take multiple HIV drugs as opposed to only taking one drug?
In terms of HIV evolution, why is it more effective to take multiple HIV drugs as opposed to only taking one drug? .
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