Delayed disease progression in HIV-2: the importance of TRIM5α and the retroviral capsid.

HIV-2 is thought to have entered the human population in the 1930s through cross-species transmission of SIV from sooty mangabeys in West Africa. Unlike HIV-1, HIV-2 has not led to a global pandemic, and recent data suggest that HIV-2 prevalence is declining in some West African states where it was formerly endemic. Although many early isolates of HIV-2 were derived from patients presenting with AIDS-defining illnesses, it was noted that a much larger proportion of HIV-2-infected subjects behaved as long-term non-progressors (LTNP) than their HIV-1-infected counterparts. Many HIV-2-infected adults are asymptomatic, maintaining an undetectable viral load for over a decade. However, despite lower viral loads, HIV-2 progresses to clinical AIDS without therapeutic intervention in most patients. In addition, successful treatment with anti-retroviral therapy (ART) is more challenging than for HIV-1. HIV-2 is significantly more sensitive to restriction by host restriction factor tripartite motif TRIM5α than HIV-1, and this difference in sensitivity is linked to differences in capsid structure. In this review we discuss the determinants of HIV-2 disease progression and focus on the important interactions between TRIM5α and HIV-2 capsid in long-term viral control.

KIR3DL1*0040102 ­ a novel three-domain KIR subtype isolated from donors of African descent.

KIR3DL1*0040102 allele differs from KIR3DL1*0040101 by a single-nucleotide change at position 12356 (intron 6).

KIR3DS1*0130109: a novel activating three-domain KIR identified using sequence-based typing.

KIR3DS1*0130109 is similar to KIR3DS1*0130101 except for a A > G change in intron 4.

Detection of a novel KIR3DL1*0150210 allele by sequencing.

KIR3DL1*0150210 has seven point mutations compared to the common Asian allele KIR3DL1*0150201.

Full-length sequence of KIR3DL1*0310102 detected in DNA samples from West Africa.

KIR3DL1*0310102 differs from KIR3DL1*0150101 with 11 nucleotide substitutions.

A novel KIR3DL1*0150103 subtype identified in West Africa.

A novel KIR3DL1*0150103 found in West Africa with five single nucleotide polymorphisms compared to KIR3DL1*0150101.

The identification of a killer cell immunoglobulin-like receptor 3DL1*0150209 in an Asian population using molecular techniques.

Full-length sequences of KIR3DL1*0150209 differ from those of KIR3DL1*0150201 with seven single-nucleotide polymorphisms.

KIR3DL1*0250103: a novel three-domain KIR allele isolated in West African samples.

The full length sequence of KIR3DL1*0250103 differs from that of KIR3DL1*0150101 with nine single-nucleotide polymorphisms.

KIR3DL1*0250102: a novel three-domain KIR subtype identified in West Africa.

KIR3DL1*0250102 differs from the common West African KIR3DL1*0150101 by 11 single nucleotide polymorphisms (SNPs).

Identification of a novel three-domain KIR allele: KIR3DL1*087 using high-resolution molecular techniques.

KIR3DL1*087 is significantly different from KIR3DL1*0010101 with multiple non-synonymous changes and insertion/deletion sites.

KIR3DS1*0130111: a novel KIR allele identified using molecular typing methods.

KIR3DS1*0130111 differs from KIR3DS1*0130101 with two previously undescribed single nucleotide polymorphisms.

HIV-exposed uninfected children: a growing population with a vulnerable immune system?

Through the successful implementation of policies to prevent mother-to-child-transmission (PMTCT) of HIV-1 infection, children born to HIV-1-infected mothers are now much less likely to acquire HIV-1 infection than previously. Nevertheless, HIV-1-exposed uninfected (HEU) children have substantially increased morbidity and mortality compared with children born to uninfected mothers (unexposed uninfected, UU), predominantly from infectious causes. Moreover, a range of phenotypical and functional immunological differences between HEU and UU children has been reported. As the number of HEU children continues to increase worldwide, two questions with clear public health importance need to be addressed: first, does exposure to HIV-1 and/or ART in utero or during infancy have direct immunological consequences, or are these poor outcomes simply attributable to the obvious disadvantages of being born into an HIV-affected household? Secondly, can we expect improved maternal care and ART regimens during and after pregnancy, together with optimized infant immunization schedules, to reduce the excess morbidity and mortality of HEU children?

Complete genomic sequence of KIR3DL1*0150102.

Full-length sequence of KIR3DL1*0150102 differs from that of KIR3DL1*0150101 in intron 6.

Description of a novel KIR3DL1*0150211 allele isolated using molecular techniques.

KIR3DL1*0150211 differs from KIR3DL1*0150201 with six single nucleotide polymorphisms in introns 3, 4, 5, and 6.

A new variant of killer-cell immunoglobulin-like receptor KIR3DL1*03101 isolated using sequence-based techniques.

The complete length genomic sequence of KIR3DL1*03101 differs from KIR3DL1*0010101 at multiple intronic and exonic sites.

Genomic full length sequence of a novel killer-cell immunoglobulin-like receptor, KIR3DL1*0010103 identified by sequencing.

KIR3DL1*0010103 differs from KIR3DL1*0010101 with four single nucleotide polymorphisms.

Isolation of full-length genomic sequences of the KIR3DL1*0040103 allele from African donors using sequence-based techniques.

The full-length genomic sequence of KIR3DL1*0040103 differs from KIR3DL1*0040101 at three nucleotide positions.

Detection of a novel killer-cell immunoglobulin-like receptor allele - KIR3DL1*0150207 - in Asian individuals.

KIR3DL1*0150207 differs from KIR3DL1*0150201 at five nucleotide positions in introns 2, 3, 4 and 5, respectively.

A novel KIR3DL1*0200102 allele isolated from a West African donor by sequence-based typing.

KIR3DL1*0200102 allele differs from KIR3DL1*0200101 with four single nucleotide polymorphisms in introns 5 and 6, respectively.

Two novel KIR3DL1 alleles, 3DL1*0150205 and 3DL1*0150206, identified by full-length DNA sequencing.

KIR3DL1*0150205 and KIR3DL1*0150206 alleles have five and six mutations, respectively, compared with KIR3DL1*0150201.