Disease severity in respiratory syncytial virus infection: Role of host genetic variation

被引:36
作者
Tahamtan, Alireza [1 ,2 ]
Askari, Fatemeh Sana [1 ]
Bont, Louis [3 ]
Salimi, Vahid [4 ]
机构
[1] Golestan Univ Med Sci, Student Res Comm, Sch Med, Gorgan, Golestan, Iran
[2] Golestan Univ Med Sci, Sch Med, Dept Microbiol, Gorgan, Golestan, Iran
[3] Univ Med Ctr Utrecht, Wilhelmina Childrens Hosp, Dept Pediat, Utrecht, Netherlands
[4] Univ Tehran Med Sci, Sch Publ Hlth, Dept Virol, Tehran, Iran
关键词
diseases severity; host genetic variation; immunopathology; nucleotide polymorphism; respiratory syncytial virus; PATTERN-RECOGNITION RECEPTORS; SINGLE NUCLEOTIDE POLYMORPHISMS; RSV BRONCHIOLITIS; PROINFLAMMATORY CYTOKINE; CD14; POLYMORPHISMS; TLR4; RANTES PROMOTER; ASSOCIATION; SUSCEPTIBILITY; INFANTS;
D O I
10.1002/rmv.2026
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Respiratory syncytial virus (RSV) infection is the most common cause of bronchiolitis and pneumonia in the pediatric population worldwide. The immunopathology of RSV infection varies considerably and severe disease occurs only in a minority of the population. There are many factors (host, viral, and environmental) that contribute to the complicated disease phenotype. In this regard, host factors are decisive for pulmonary susceptibility to RSV infection. Host genetic diversity certainly affects the balance between control of viral replication and tissue damage during RSV infection, consequently impacting on diseases outcome. In this review, we discuss the role of host genetic variation in disease caused by RSV aiming to highlight genetic risk factors for one of the most common diseases in early childhood. Our findings clearly indicate that the response of each individual to infection is influenced by genetic diversity mainly linked to the regulation of host immune responses. Future genetic association and functional studies using more powerful and consistently reproducible approaches will likely be able to confirm, refine, and expand our developing concept of RSV disease pathogenesis.
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页数:15
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