Abstract
Human adenovirus type 55 (HAdV-55) is considered a highly virulent pathogen causing severe and even deadly pneumonia in immunocompetent people. The mechanisms of HAdV-55-induced initiation and progression of severe pneumonia remain ambiguous. In the current study, we endeavored to identify novel immune response genes which are substantially involved in the pathogenesis of severe inflammation in HAdV-55-infected patients. HAdV-55-infected patients with upper respiratory tract symptoms (minor patients) and pneumonia (severe patients) were enrolled. Through transcriptome sequencing and quantitative real-time PCR, the peripheral blood mononuclear cells of the patients were analyzed. We found that the expression of eight genes, including Il18, Il36b, Il17rc, Tnfsf10, Tnfsf11, Tnfsf14, Tnfsf15, and Il1a, were closely correlated with the severity of HAdV-55 infection. Most of these genes belong to interleukin-1 family or tumor necrosis factor (TNF) superfamily, respectively. The changes in gene expression were confirmed by Western blot assay. Our data will be crucial for deepening the understanding of the pathogenic mechanisms of severe pneumonia in HAdV-55 infection.
Highlights
Adenoviruses are a class of double-stranded DNA viruses infecting the respiratory tract, eyes, intestines, urinary tract, and nervous system (Khanal et al, 2018)
We found that the expression of eight genes, including Il18, Il36b, Il17rc, Tnfsf10, Tnfsf11, Tnfsf14, Tnfsf15, and Il1a, were closely correlated with the severity of Human adenovirus type 55 (HAdV-55) infection
In the following gene expression analysis, we mainly focused on the genes of which the expression was up-regulated
Summary
Adenoviruses are a class of double-stranded DNA viruses infecting the respiratory tract, eyes, intestines, urinary tract, and nervous system (Khanal et al, 2018). HAdV-55 has a recombinant genome from HAdV-B11 which is a renal pathogen with the antigenic epitope, and HAdV-B14 which is a respiratory pathogen conferring the cell tropism, biological and pathological properties (Walsh et al, 2010). From 2004 to 2006, three major outbreaks of HAdV-55 infection took place in Turkey, Singapore, and China mainland, eliciting nearly 1000 patients and 2 deaths (Sun et al, 2014). Other recent outbreaks are reported (Girouard et al, 2011; Zhao et al, 2014). Since the discovery of HAdV-55, several laboratory investigations have addressed the viral biology such as its genome and clinical manifestations after infection.
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