Gag and Nef, were also found to be the most frequently targeted proteins by CD4+ T cells in clade B HIV-1 infection and in the less pathogenic HIV-2 infection [20], [31].
The emergence of a possible highly pathogenic HIV-2 strain is an ongoing concern, given that retroviruses can easily evolve to evade host defenses.
The CD3-TCR complex is known to participate in the mechanism responsible for different levels of immune activation and T-cell apoptosis in pathogenic HIV-human and nonpathogenic SIV-monkey infections [ 45, 46].
This study aims to test the serial passage theory of HIV emergence and elucidate adaptive mechanisms to a new host using the newly emerged, pathogenic HIV-2F virus in an in vivo pigtail macaque (PTM) model.
One feature of pathogenic HIV-1 infection that distinguishes it from non-pathogenic SIV infections is the high level of chronic immune activation associated with accelerated T-cell turnover rates and apoptosis [ 5].
Published data describe HIV-1 to be more pathogenic than HIV-2, HIV-1 subtype D to be more pathogenic than subtype A [15 17,19 23], and subtype C more pathogenic than A and D [24].
Although less transmissible and less pathogenic than HIV-1 [ 7– 12], HIV-2 nevertheless kills 2 3% of infected individuals, each year [ 9].
HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution.
