The role of host genetic factors in respiratory tract infectious diseases: systematic review, meta-analyses and field synopsis

Chagas disease, which is caused by the flagellate parasiteTrypanosoma cruzi, affects 8–10 million people in Latin America. The disease is endemic and is characterised by acute and chronic phases that develop in the indeterminate, cardiac, and/or gastrointestinal forms. The immune response during humanT. cruziinfection is not completely understood, despite its role in driving the development of distinct clinical manifestations of chronic infection. Polymorphisms in genes involved in the innate and specific immune response are being widely studied in order to clarify their possible role in the occurrence or severity of disease. Here we review the role of classic and nonclassic MHC,KIR, and cytokine host genetic factors on the infection byT. cruziand the clinical course of Chagas disease.

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A systematic review and meta-analysis of host genetic factors associated with influenza severity

BMC Genomics ◽

10.1186/s12864-021-08240-7 ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Nina Van Goethem ◽

Célestin Danwang ◽

Nathalie Bossuyt ◽

Herman Van Oyen ◽

Nancy H. C. Roosens ◽

...

Keyword(s):

Systematic Review ◽

Genetic Factors ◽

Association Studies ◽

Influenza Infection ◽

Meta Analysis ◽

Genetic Association Studies ◽

Genome Wide Association Studies ◽

Severe Influenza ◽

Host Genetic ◽

Host Genetic Factors

Abstract Background The severity of influenza disease can range from mild symptoms to severe respiratory failure and can partly be explained by host genetic factors that predisposes the host to severe influenza. Here, we aimed to summarize the current state of evidence that host genetic variants play a role in the susceptibility to severe influenza infection by conducting a systematic review and performing a meta-analysis for all markers with at least three or more data entries. Results A total of 34 primary human genetic association studies were identified that investigated a total of 20 different genes. The only significant pooled ORs were retrieved for the rs12252 polymorphism: an overall OR of 1.52 (95% CI [1.06–2.17]) for the rs12252-C allele compared to the rs12252-T allele. A stratified analysis by ethnicity revealed opposite effects in different populations. Conclusion With exception for the rs12252 polymorphism, we could not identify specific genetic polymorphisms to be associated with severe influenza infection in a pooled meta-analysis. This advocates for the use of large, hypothesis-free, genome-wide association studies that account for the polygenic nature and the interactions with other host, pathogen and environmental factors.

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HLA-B∗57 and Gender Influence the Occurrence of Tuberculosis in HIV Infected People of South India

Clinical and Developmental Immunology ◽

10.1155/2011/549023 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 5

Author(s):

Latha Jagannathan ◽

Mrinalini Chaturvedi ◽

Bhuthaiah Satish ◽

Kadappa Shivappa Satish ◽

Anita Desai ◽

...

Keyword(s):

South India ◽

Genetic Factors ◽

Infected People ◽

Gender Influence ◽

Hiv Positive Women ◽

Host Genetic ◽

And Gender ◽

Hiv Seropositive ◽

Host Genetic Factors

Background. Substantial evidence exists for HLA and other host genetic factors being determinants of susceptibility or resistance to infectious diseases. However, very little information is available on the role of host genetic factors in HIV-TB coinfection. Hence, a longitudinal study was undertaken to investigate HLA associations in a cohort of HIV seropositive individuals with and without TB in Bangalore, South India.Methods. A cohort of 238 HIV seropositive subjects were typed for HLA-A, B, and DR by PCR-SSP and followed up for 5 years or till manifestation of Tuberculosis. HLA data of 682 HIV Negative healthy renal donors was used as control.Results. The ratio of males and females in HIV cohort was comparable (50.4% and 49.6%). But the incidence of TB was markedly lower in females (12.6%,) than males (25.6%). Further, HLA-B*57 frequency in HIV cohort was significantly higher among females without TB (21.6%, 19/88) than males (1.7%, 1/59);P=0.0046;OR=38. CD4 counts also were higher among females in this cohort.Conclusion. This study suggests that HIV positive women with HLA-B*57 have less occurrence of TB as compared to males.

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A systematic review of the Trypanosoma cruzi genetic heterogeneity, host immune response and genetic factors as plausible drivers of chronic chagasic cardiomyopathy

Parasitology ◽

10.1017/s0031182018001506 ◽

2018 ◽

Vol 146 (3) ◽

pp. 269-283 ◽

Cited By ~ 5

Author(s):

Paula Jiménez ◽

Jesús Jaimes ◽

Cristina Poveda ◽

Juan David Ramírez

Keyword(s):

Systematic Review ◽

Immune Response ◽

Trypanosoma Cruzi ◽

Virulence Factors ◽

Genetic Heterogeneity ◽

Genetic Factors ◽

International Consensus ◽

Host Genetic ◽

Chagasic Cardiomyopathy ◽

Host Genetic Factors

AbstractChagas disease is a complex tropical pathology caused by the kinetoplastid Trypanosoma cruzi. This parasite displays massive genetic diversity and has been classified by international consensus in at least six Discrete Typing Units (DTUs) that are broadly distributed in the American continent. The main clinical manifestation of the disease is the chronic chagasic cardiomyopathy (CCC) that is lethal in the infected individuals. However, one intriguing feature is that only 30–40% of the infected individuals will develop CCC. Some authors have suggested that the immune response, host genetic factors, virulence factors and even the massive genetic heterogeneity of T. cruzi are responsible of this clinical pattern. To date, no conclusive data support the reason why a few percentages of the infected individuals will develop CCC. Therefore, we decided to conduct a systematic review analysing the host genetic factors, immune response, cytokine production, virulence factors and the plausible association of the parasite DTUs and CCC. The epidemiological and clinical implications are herein discussed.

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Genetic aspects of inflammation and cancer

Biochemical Journal ◽

10.1042/bj20071341 ◽

2008 ◽

Vol 410 (2) ◽

pp. 225-235 ◽

Cited By ~ 69

Author(s):

Georgina L. Hold ◽

M. Emad El-Omar

Keyword(s):

Chronic Inflammation ◽

Genetic Factors ◽

Therapeutic Strategies ◽

Signalling Pathways ◽

Neoplastic Progression ◽

Comprehensive Understanding ◽

Host Genetic ◽

Host Genetic Factors ◽

Pro Inflammatory Cytokines

Chronic inflammation is involved in the pathogenesis of most common cancers. The aetiology of the inflammation is varied and includes microbial, chemical and physical agents. The chronically inflamed milieu is awash with pro-inflammatory cytokines and is characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process, promoting neoplastic progression but also facilitating cancer prevention. A comprehensive understanding of the molecular and cellular inflammatory mechanisms involved is vital for developing preventive and therapeutic strategies against cancer. The purpose of the present review is to evaluate the mechanistic pathways that underlie chronic inflammation and cancer with particular emphasis on the role of host genetic factors that increase the risk of carcinogenesis.

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