Genetic Markers of the Host in Persons Living with HTLV-1, HIV and HCV Infections

Assone, Tatiane; Paiva, Afonso; Fonseca, Luiz Augusto Marcondes; Casseb, Jorge

doi:10.3390/v8020038

Cited by 19 publications

(10 citation statements)

References 126 publications

(157 reference statements)

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“…Six of 9 patients carried HLA-B allele B*57 or B*52, associated with slow clinical progression [ 55 – 57 ]. Two individuals were heterozygotes for CCR5Δ32 deletion, also described as a protective factor [ 56 ]. EC17, VC14, and EC42 did not carry an HLA-B allele or exhibit a CCR5 genetic profile associated with the control of viral replication and/or non-progression to AIDS.…”

Section: Resultsmentioning

confidence: 99%

Next-generation sequencing analyses of the emergence and maintenance of mutations in CTL epitopes in HIV controllers with differential viremia control

et al. 2018

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BackgroundDespite the low level of viral replication in HIV controllers (HICs), studies have reported viral mutations related to escape from cytotoxic T-lymphocyte (CTL) response in HIV-1 plasma sequences. Thus, evaluating the dynamics of the emergence of CTL-escape mutants in HICs reservoirs is important for understanding viremia control. To analyze the HIV-1 mutational profile and dynamics of CTL-escape mutants in HICs, we selected 11 long-term non-progressor individuals and divided them into the following groups: (1) viremic controllers (VCs; n = 5) and (2) elite controllers (ECs; n = 6). For each individual, we used HIV-1 proviral DNA from PBMCs related to earliest (VE) and latest (VL) visits to obtain gag and nef sequences using the Illumina HiSeq system. The consensus of each mapped gene was used to assess viral divergence, and next-generation sequencing data were employed to identify SNPs and variations within and flanking CTL epitopes.ResultsDivergence analysis showed higher values for nef compared to gag among the HICs. EC and VC groups showed similar divergence rates for both genes. Analysis of the number of SNPs showed that VCs present more variability in both genes. Synonymous/non-synonymous mutation ratios were < 1 for gag among ECs and for nef among ECs and VCs, exhibiting a predominance of non-synonymous mutations. Such mutations were observed in regions encoding CTL-restricted epitopes in all individuals. All ECs presented non-synonymous mutations in CTL epitopes but generally at low frequency (< 1%); all VCs showed a high number of mutations, with significant frequency changes between VE and VL visits. A higher frequency of internal mutations was observed for gag epitopes, with significant changes across visits compared to Nef epitopes, indicating a pattern associated with differential genetic pressure.ConclusionsThe high genetic conservation of HIV-1 gag and nef among ECs indicates that the higher level of viremia control restricts the evolution of both genes. Although viral replication levels in HICs are low or undetectable, all individuals exhibited CTL epitope mutations in proviral gag and nef variants, indicating that potential CTL escape mutants are present in HIC reservoirs and that situations leading to a disequilibrium of the host-virus relationship can result in the spread of CTL-escape variants.Electronic supplementary materialThe online version of this article (10.1186/s12977-018-0444-z) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Next-generation sequencing analyses of the emergence and maintenance of mutations in CTL epitopes in HIV controllers with differential viremia control

et al. 2018

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“…This proviral load depends on the strength of an individual's cytotoxic T-lymphocyte response to HTLV-1, which is associated with the genetically determined human leucocyte antigen (HLA) class 1 types. Associations have indeed been found between specific HLA types and the proviral load (e.g., HLA-A * 02), HAM/TSP (e.g., HLA-DRB1 * 0101), and ATLL (e.g., HLA-A * 26) (Jeffery et al, 1999; Sonoda et al, 2011; Assone et al, 2016). These associations, however, could not be replicated across populations (Talledo et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Family Aggregation of Human T-Lymphotropic Virus 1-Associated Diseases: A Systematic Review

Álvarez¹,

Gotuzzo

Vandamme

et al. 2016

Front. Microbiol.

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Human T-lymphotropic virus 1 (HTLV-1) is a retrovirus that produces a persistent infection. Two transmission routes (from mother to child and via sexual intercourse) favor familial clustering of HTLV-1. It is yet unknown why most HTLV-1 carriers remain asymptomatic while about 10% of them develop complications. HTLV-1 associated diseases were originally described as sporadic entities, but familial presentations have been reported. To explore what is known about family aggregation of HTLV-1-associated diseases we undertook a systematic review. We aimed at answering whether, when, and where family aggregation of HTLV-1-associated diseases was reported, which relatives were affected and which hypotheses were proposed to explain aggregation. We searched MEDLINE, abstract books of HTLV conferences and reference lists of selected papers. Search terms used referred to HTLV-1 infection, and HTLV-1-associated diseases, and family studies. HTLV-1-associated diseases considered are adult T-cell leukemia/lymphoma (ATLL), HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), HTLV-1-associated uveitis, and infective dermatitis. Seventy-four records reported HTLV-1-associated diseases in more than one member of the same family and were included. Most reports came from HTLV-1-endemic countries, mainly Japan (n = 30) and Brazil (n = 10). These reports described a total of 270 families in which more than one relative had HTLV-1-associated diseases. In most families, different family members suffered from the same disease (n = 223). The diseases most frequently reported were ATLL (115 families) and HAM/TSP (102 families). Most families (n = 144) included two to four affected individuals. The proportion of ATLL patients with family history of ATLL ranged from 2 to 26%. The proportion of HAM/TSP patients with family history of HAM/TSP ranged from 1 to 48%. The predominant cluster types for ATLL were clusters of siblings and parent-child pairs and for HAM/TSP, an affected parent with one or more affected children. The evidence in the literature, although weak, does suggest that HTLV-1-associated diseases sometimes cluster in families. Whether familial transmission of HTLV-1 is the only determining factor, or whether other factors are also involved, needs further research.

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“…Although HIV-1, HTLV-1/-2, HBV, and HCV share some common routes of infection, the risks of acquiring these infectious agents vary considerably in Brazil, and are dependent on the genetic backgrounds of individuals, geographic region, socioeconomic conditions, and risk behaviours ( Catalan-Soares et al 2005 , Pereira et al 2013 , Ximenes et al 2015 , MS 2016a , b , Assone et al 2016 ).…”

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confidence: 99%

Making the invisible visible: searching for human T-cell lymphotropic virus types 1 and 2 (HTLV-1 and HTLV-2) in Brazilian patients with viral hepatitis B and C

Caterino–de–Araujo

Alves

Campos

et al. 2018

Mem. Inst. Oswaldo Cruz

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With this study, the authors hope to alert clinicians regarding the presence of human T-cell lymphotropic virus type 1 and 2 (HTLV-1/-2) infections in patients with viral hepatitis B and C in Brazil. HTLV-1/-2 were detected in 1.3% of hepatitis B virus (HBV)- and 5.3% of hepatitis C virus (HCV)-infected blood samples sent for laboratory viral load measurements. A partial association of human immunodeficiency virus (HIV)-1 and HTLV-1/-2 infection was detected in patients with HCV (HIV+, 27.3%), whereas this association was almost 100% in HBV-infected patients (HIV+, all except one). The high prevalence of HTLV-1/-2 infection among patients with hepatitis C was of concern, as HTLV-1/-2 could change the natural course of subsequent liver disease. The authors suggest including HTLV-1/-2 serology in the battery of tests used when following patients with viral hepatitis in Brazil, regardless of the HIV status.

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Genetic Markers of the Host in Persons Living with HTLV-1, HIV and HCV Infections

Cited by 19 publications

References 126 publications

Next-generation sequencing analyses of the emergence and maintenance of mutations in CTL epitopes in HIV controllers with differential viremia control

Next-generation sequencing analyses of the emergence and maintenance of mutations in CTL epitopes in HIV controllers with differential viremia control

Family Aggregation of Human T-Lymphotropic Virus 1-Associated Diseases: A Systematic Review

Making the invisible visible: searching for human T-cell lymphotropic virus types 1 and 2 (HTLV-1 and HTLV-2) in Brazilian patients with viral hepatitis B and C

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