Abstract
The polymorphism of human leukocyte antigen (HLA), which is a genetic factor that influences the progression of hemorrhagic fever with renal syndrome (HFRS) after Hantaan virus (HTNV) infection, was incompletely understood. In this case-control study, 76 HFRS patients and 370 healthy controls of the Chinese Han population were typed for the HLA-A, -B, and -DRB1 loci. The general variation at the HLA-DRB1 locus was associated with the onset of HFRS (P < 0.05). The increasing frequencies of HLA-DRB1∗09 and HLA-B∗46-DRB1∗09 in HFRS patients were observed as reproducing a previous study. Moreover, the HLA-B∗51-DRB1∗09 was susceptible to HFRS (P = 0.037; OR = 3.62; 95% CI: 1.00–13.18). The increasing frequencies of HLA-B∗46, HLA-B∗46-DRB1∗09, and HLA-B∗51-DRB1∗09 were observed almost in severe/critical HFRS patients. The mean level of maximum serum creatinine was higher in HLA-B∗46-DRB1∗09 (P = 0.011), HLA-B∗51-DRB1∗09 (P = 0.041), or HLA-B∗46 (P = 0.011) positive patients than that in the negative patients. These findings suggest that the allele HLA-B∗46 and haplotypes HLA-B∗46-DRB1∗09 and HLA-B∗51-DRB1∗09 in patients could contribute to a more severe degree of HFRS and more serious kidney injury, which improve our understanding of the HLA polymorphism for a different outcome of HTNV infection.
Highlights
Hantaan virus (HTNV), the prototype member of the Hantavirus genus, causes hemorrhagic fever with renal syndrome (HFRS) in humans
These findings suggest that the allele human leukocyte antigen (HLA)-B∗46 and haplotypes HLA-B∗46-DRB1∗09 and HLA-B∗51-DRB1∗09 in patients could contribute to a more severe degree of HFRS and more serious kidney injury, which improve our understanding of the HLA polymorphism for a different outcome of HTNV infection
The HLADRB1 loci consisted significantly of more polymorphisms in HFRS patients (P = 0.049), but the polymorphism in the HLA-A or -B genes showed no difference from the normal controls. These findings suggest that HLA-DRB1 was the major locus with polymorphisms that were probably related to the occurrence and disease progression of HFRS patients in the Chinese Han population
Summary
Hantaan virus (HTNV), the prototype member of the Hantavirus genus, causes hemorrhagic fever with renal syndrome (HFRS) in humans. Hantaviruses are enveloped negativesense RNA viruses that belong to the family Bunyaviridae. They are rodent-borne viruses and are transmitted to humans primarily from aerosols of rodent excreta [1, 2]. People who get infected with HTNV are clinically characterized by sudden fever, hemorrhage, thrombocytopenia, and acute renal failure, leading from an asymptomatic to a severe, lifethreatening illness. The pathogenic HTNV infection emerged as an increasing threat to human health with 60,000–100,000 cases worldwide reported annually and a case fatality rate of 6.04% [3, 4]. The mechanisms underlying the different severities of HFRS are not yet understood
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