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Hantaan Virus Infection Induces Both Th1 and ThGranzyme B+ Cell Immune Responses That Associated with Viral Control and Clinical Outcome in Humans


Hantaan virus (HTNV), the prototype of Hantavirus genus, is a rodent-borne pathogen that causes human hemorrhagic fever with renal syndrome, with mortality rate of approximately 15% in Asia. The efforts of our immune system to defend against HTNV are important for clearance of the infection. However, the interaction between CD4+T-cell immunity and HTNV infection in humans is not known. Based on the novel T-cell epitopes we defined on HTNV glycoprotein in Chinese Han population, we confirmed that HTNV glycoprotein could induce vigorous and extensive CD4+T-cell response in humans. For the first time, we showed that both Th1 and ThGranzyme B+ cell responses involved in defense against HTNV infection and inversely correlated with plasma viral load and disease outcome. Additionally, we found that CD4+T cells characterized by broader antigenic repertoire, polyfunctional cytokine secretion, stronger expansion and highly differentiated effector memory phenotype always lead to much milder outcome of the disease, maybe through inducing antiviral condition of host cells and cytotoxic effect of ThGranzyme B+ cells. Our results add weight to the contribution of CD4+T cells in disease control after HTNV infection in humans, which may greatly advance the understanding about how HTNV interact with their host organisms.


Vyšlo v časopise: Hantaan Virus Infection Induces Both Th1 and ThGranzyme B+ Cell Immune Responses That Associated with Viral Control and Clinical Outcome in Humans. PLoS Pathog 11(4): e32767. doi:10.1371/journal.ppat.1004788
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004788

Souhrn

Hantaan virus (HTNV), the prototype of Hantavirus genus, is a rodent-borne pathogen that causes human hemorrhagic fever with renal syndrome, with mortality rate of approximately 15% in Asia. The efforts of our immune system to defend against HTNV are important for clearance of the infection. However, the interaction between CD4+T-cell immunity and HTNV infection in humans is not known. Based on the novel T-cell epitopes we defined on HTNV glycoprotein in Chinese Han population, we confirmed that HTNV glycoprotein could induce vigorous and extensive CD4+T-cell response in humans. For the first time, we showed that both Th1 and ThGranzyme B+ cell responses involved in defense against HTNV infection and inversely correlated with plasma viral load and disease outcome. Additionally, we found that CD4+T cells characterized by broader antigenic repertoire, polyfunctional cytokine secretion, stronger expansion and highly differentiated effector memory phenotype always lead to much milder outcome of the disease, maybe through inducing antiviral condition of host cells and cytotoxic effect of ThGranzyme B+ cells. Our results add weight to the contribution of CD4+T cells in disease control after HTNV infection in humans, which may greatly advance the understanding about how HTNV interact with their host organisms.


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