Association of human leukocyte antigen class II allele and haplotypes in chikungunya viral infection in a western Indian population

Thanapati, Subrat; Hande, Aparna; Das, Rumki; Gurav, Yogesh K.; Tripathy, Anuradha S.

doi:10.1093/trstmh/tru030

Cited by 13 publications

(11 citation statements)

References 27 publications

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“…Similarly, haplotypes DRB1*04, DRB1*03, DRB1*08, DRB1*09 and DRB1*11 are abundant in our class II specific epitopes. These haplotypes were seen to be associated with zoonotic viral infection [80, 81]. …”

Section: Discussionmentioning

confidence: 99%

Insight into SNPs and epitopes of E protein of newly emerged genotype-I isolates of JEV from Midnapur, West Bengal, India

2017

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BackgroundJapanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes Japanese Encephalitis (JE) and Acute Encephalitis Syndrome (AES) in humans. Genotype-I (as co-circulating cases with Genotype-III) was isolated in 2010 (JEV28, JEV21) and then in 2011 (JEV45) from Midnapur district, West Bengal (WB) for the first time from clinical patients who were previously been vaccinated with live attenuated SA14-14-2 strain. We apply bioinformatics and immunoinformatics on sequence and structure of E protein for analysis of crucial substitutions that might cause the genotypic transition, affecting proteinfunction and altering specificity of epitopes.ResultsAlthough frequency of substitutions in E glycoprotein of JEV28, JEV21 and JEV45 isolates vary, its homologous patterns remain exactly similar as earlier Japan isolate (Ishikawa). Sequence and 3D model-structure based analyses of E protein show that only four of all substitutions are critical for genotype-I specific effect of which N103K is common among all isolates indicating its role in the transition of genotype-III to genotype-I. Predicted B-cell and T-cell epitopes are seen to harbor these critical substitutions that affect overall conformational stability of the protein. These epitopes were subjected to conservation analyses using a large set of the protein from Asian continent.ConclusionsThe study identifies crucial substitutions that contribute to the emergence of genotype-I. Predicted epitopes harboring these substitutions may alter specificity which might be the reason of reported failure of vaccine. Conservation analysis of these epitopes would be useful for design of genotype-I specific vaccine.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-017-0197-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Insight into SNPs and epitopes of E protein of newly emerged genotype-I isolates of JEV from Midnapur, West Bengal, India

2017

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“…The DRB1 * 07 allele is associated with protection against Dengue virus infection in the Cuban population, but not in the Sri Lankan population ( 79 , 80 ). Studies have demonstrated HLA class II alleles association to susceptibility or resistance to CHIKV ( Table 1 , Figure 2 ), however none have reported associations with clinical symptoms of CHIKV infection ( 78 , 81 , 82 ).…”

Section: Host Genetics and Chikungunyamentioning

confidence: 99%

Section: Host Genetics and Chikungunyamentioning

confidence: 99%

“…In India, two studies have reported the association of HLA alleles with CHIKV infection ( 78 , 81 ). One study demonstrated the presence of HLA-DRB1 * 04-HLA-DQB1 * 03 haplotype with susceptibility to CHIKV infection, and the presence of HLA-DRB1 * 11 and HLA-DRB1 * 11-HLA-DQB1 * 03 haplotype with resistance to the infection ( 81 ). According to the authors, one explanation could be that the epitopes presented by HLA-DRB * 11 modulates toward a more robust immune response to CHIKV by means of CD4 T cells.…”

Section: Host Genetics and Chikungunyamentioning

confidence: 99%

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Human Genetic Host Factors and Its Role in the Pathogenesis of Chikungunya Virus Infection

et al. 2022

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Chikungunya virus (CHIKV) is an alphavirus from the Togaviridae family that causes acute arthropathy in humans. It is an arthropod-borne virus transmitted initially by the Aedes (Ae) aegypti and after 2006's epidemic in La Reunion by Ae albopictus due to an adaptive mutation of alanine for valine in the position 226 of the E1 glycoprotein genome (A226V). The first isolated cases of CHIKV were reported in Tanzania, however since its arrival to the Western Hemisphere in 2013, the infection became a pandemic. After a mosquito bite from an infected viremic patient the virus replicates eliciting viremia, fever, rash, myalgia, arthralgia, and arthritis. After the acute phase, CHIKV infection can progress to a chronic stage where rheumatic symptoms can last for several months to years. Although there is a great number of studies on the pathogenesis of CHIKV infection not only in humans but also in animal models, there still gaps in the proper understanding of the disease. To this date, it is unknown why a percentage of patients do not develop clinical symptoms despite having been exposed to the virus and developing an adaptive immune response. Also, controversy stills exist on the pathogenesis of chronic joint symptoms. It is known that host immune response to an infectious disease is reflected on patient's symptoms. At the same time, it is now well-established that host genetic variation is an important component of the varied onset, severity, and outcome of infectious disease. It is essential to understand the interaction between the aetiological agent and the host to know the chronic sequelae of the disease. The present review summarizes the current findings on human host genetics and its relationship with immune response in CHIKV infection.

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“…These polymorphisms allow the immune system to increase the repertoire of peptides presented by HLA molecules, which in turn will affect the host's susceptibility to infectious diseases. There is evidence that HLA class II alleles are associated with susceptibility or resistance to CHIKV; however, no association has been reported with clinical symptoms of CHIKV infection (Bouquillard & Combe, 2009; Chaaithanya et al., 2013; Thanapati et al., 2014). There is a lack of evidence of association studies of HLA class I and II alleles in the Latin American CHIKV epidemic.…”

Section: Introductionmentioning

confidence: 99%

Can presence of HLA type I and II alleles be associated with clinical spectrum of CHIKV infection?

Rueda

Santos

Angarita

et al. 2021

Transbounding Emerging Dis

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Host immune response and virulence factors are key to disease susceptibility. However, there are no known association studies of human leukocyte antigen (HLA) class I and II alleles with chikungunya virus (CHIKV) infection in the Latin American population. Here, we aimed to identify HLA alleles present in patients with CHIKV infection versus healthy controls as well as the allelic association with the clinical spectrum of the disease. We conducted a cross‐sectional analysis of a community cohort and included patients aged 18 years and older with serologically confirmed CHIKV infection. HLA typing of HLA‐A, HLA‐B, and HLA‐DRB1 alleles was performed. Two‐by‐two tables were used to establish associations between allele presence and clinical characteristics. Data from 65 patients with confirmed CHIKV infection were analyzed for HLA typing. CHIKV infection was significantly associated with the presence of HLA‐A*68 [p = .005; odds ratio (OR): 8.90; 95% confidence interval (CI): 1.88–42.13], HLA‐B*35 (p = .03; OR: 2.01; 95% CI: 1.06–3.86), HLA‐DRB*01 (p <.001; OR: 5.70; 95% CI: 1.95–16.59), HLA‐DRB1*04 (p <.001; OR: 7.37; 95% CI: 3.33–16.30), and HLA‐DRB1*13 (p = .004; OR: 3.75; 95% CI: 1.50–9.39) alleles in patients versus healthy subjects. A statistically significant relationship was found between the presence of a rash on the face or abdomen and the presence of HLA‐DRB1*04 (p = .028; OR: 3.2; 95% CI: 1.11–9.15 and p = .007; OR: 4.33; 95% CI: 1.45–12.88, respectively). Our study demonstrated that, in our cohort, HLA type I and type II alleles are associated with CHIKV infection, and an HLA type II allele is associated with dermatological symptoms. Further research is needed to establish a path for future investigation of genes outside the HLA system to improve knowledge of the pathophysiology of CHIKV infection and its host–pathogen interaction.

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Association of human leukocyte antigen class II allele and haplotypes in chikungunya viral infection in a western Indian population

Cited by 13 publications

References 27 publications

Insight into SNPs and epitopes of E protein of newly emerged genotype-I isolates of JEV from Midnapur, West Bengal, India

Insight into SNPs and epitopes of E protein of newly emerged genotype-I isolates of JEV from Midnapur, West Bengal, India

Human Genetic Host Factors and Its Role in the Pathogenesis of Chikungunya Virus Infection

Can presence of HLA type I and II alleles be associated with clinical spectrum of CHIKV infection?

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