Impact of Human Leukocyte Antigen Polymorphisms in Human Immunodeficiency Virus Progression in a Paediatric Cohort Infected with a Mono-phyletic Human Immunodeficiency Virus-1 Strain

Montesano, Carla; Bonanno, Cesira T.; Grifoni, Alba; Sano, Caterina Di; Gattinara, Guido Castelli; Mattei, Maurizio; Mancino, Giorgio; Salerno, Alfredo; Colizzi, Vittorio; Amicosante, Massimo

doi:10.4172/2155-6113.1000282

Cited by 3 publications

(7 citation statements)

References 27 publications

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“…All the children were infected after attending the outpatient service of the hospital or while being hospitalized at least once. The HIV and other blood‐borne infections, the outbreak, and immunological and immunogenetic characterizations of the cohort have been previously described, indicating in the cohort the presence of a defined cluster of HIV‐1 clade A/G virus (CRF02_AG).…”

Section: Methodsmentioning

confidence: 86%

“…HLA typing and HIV‐1 Gag, Vif, Vpr and Tat gene sequencing were performed upon residual blood samples, after informed consent, in a subgroup of 107 HIV‐1‐infected children from the cohort.…”

Section: Methodsmentioning

confidence: 99%

“…High‐resolution HLA‐A, ‐B and ‐DRB1 typing was performed as previously reported . HIV‐1 Gag, Vif, Vpr and Tat sequences and HCV E1/E2 sequence were obtained as previously described .…”

Section: Methodsmentioning

confidence: 99%

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Role of individual's T‐cell immunome in controlling HIV‐1 progression

et al. 2014

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SummaryViral and host factors can influence HIV-1 progression, among them human leucocyte antigen (HLA) has shown the strongest effect. However, studies on the functional contribution of HLA in controlling HIV progression toward AIDS are limited by multiple issues, including the viral strain variability within the study subjects. In this study, in a cohort of children infected with a monophyletic strain (CRF02_AG) during an outbreak, we evaluated the HIV-1 Gag, Vif, Vpr, Tat and hepatitis C virus E1/E2 (as control) proteins circulating in a cohort for the capability to be presented by the HLA molecules in the same population. A total of 70 Non-progressors and 37 Progressors to AIDS were evaluated. In the presence of a constant capability of HIV-1 to mutate in the region containing epitopes of Gag protein, the number of epitopes recognized in silico by the combination of the HLA alleles along the Gag consensus sequence is significantly higher in the Non-progressors compared with Progressors (HLA-A:Non-progressors = 1Á532 AE 1Á211, Progressors = 0Á7714 AE 1Á031, P = 0Á0016; HLA-B: Non-progressors = 1Á556 AE 1Á298, Progressors = 1Á000 AE 0Á817, P = 0Á0319; HLA-DR: Non-progressors = 13Á30 AE 9Á488, Progressors = 7Á294 AE 6Á952, P = 0Á0006). Similar results were obtained for the other HIV-1 proteins Vif and Vpr, whereas no differences were obtained in the number of epitopes for the hepatitis C virus E1/E2 protein sequence or for the scrambled HIV-1 sequence. Finally, the results were confirmed also in a subgroup of subjects where both HLA typing and Gag sequence were available. In conclusion, in the absence of bias due to viral strain diversity, it is the overall fitting of the HLA molecules that are capable of better binding HIV-1 proteins in determining the major role in the control of HIV-1 replication and progression to AIDS.

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Section: Methodsmentioning

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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Role of individual's T‐cell immunome in controlling HIV‐1 progression

et al. 2014

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“…All the children were infected after hospitalization or after attending the hospital outpatients'. The HIV infection, outbreak, immunological, and immunogenetics characterizations of the cohort have been previously described [ 17 , 20 – 22 ], indicating in the cohort the presence of a defined cluster of HIV-1 clade A/G virus (CRF02_AG).…”

Section: Methodsmentioning

confidence: 99%

HS1,2 Ig Enhancer Alleles Association to AIDS Progression in a Pediatric Cohort Infected with a Monophyletic HIV-Strain

Montesano

Giambra

Frezza

et al. 2014

BioMed Research International

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Alteration in the humoral immune response has been observed during HIV infection. The polymorphisms of enhancer HS1,2, member of the 3′ regulatory region of the Ig heavy chain cluster, may play a role in the variation of the humoral response leading to pathological conditions. To assess the role of the HS1,2 polymorphic variants in the progression of AIDS, the HS1,2-A allelic frequencies were investigated in a cohort of HIV infected pediatric subjects from a nosocomial outbreak with a monophyletic strain of HIV. From a total group of 418 HIV infected children in the outbreak cohort, 42 nonprogressors and 31 progressors without bias due to antiretroviral therapy were evaluated. HS1,2 allele ∗1 has been associated with nonprogressors (allelic frequency: 51.19% versus 33.87% in progressors, OR 0.5, and P = 0.0437), while allele ∗2 has been associated with progression (allelic frequency: 48.39% versus 30.95% in nonprogressors, OR 2.1, and P = 0.0393). Further, only subjects carrying allele ∗2 in absence of allele ∗1, either in homozygous condition for allele ∗2 [nonprogressors 2/42 (4.76%), Progressors 7/31 (22.58%), OR 5.8, and P = 0.0315] or in combination with other allelic variants [nonprogressors 7/42 (16.67%), Progressors 13/31 (41.93%), OR 3.61, and P = 0.0321], have been associated with HIV progression to AIDS. In conclusion, while the HS1,2 allele ∗1 has a protective effect on HIV progression when present, allele ∗2 is associated with progression toward AIDS when allele ∗1 is absent.

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“…It is well known that HIV-specific T-cell response, and in particular Cytotoxic T lymphocyte , plays a key role in controlling HIV infection [44,45] As the T-cell response is dictated by HLA molecules, the individual's variation in the HLA class I and II alleles has a profound effect on the outcome of infection and disease progression to AIDS [45,46]. The interaction of NK's inhibitory receptor with HLA regulate innate immune response and might have important implications for a better disease control [47]. In addition, some specific combination of HLA-B*44 with KIR alleles might be at the basis of the prevention of HIV infection in the mother to child transmission as already described for HIV progression [48].…”

Section: Discussionmentioning

confidence: 99%