Immunopathogenesis of Different Emerging Viral Infections: Evasion, Fatal Mechanism, and Prevention

Abstract

Different emerging viral infections may emerge in different regions of the world and pose a global pandemic threat with high fatality. Clarification of the immunopathogenesis of different emerging viral infections can provide a plan for the crisis management and prevention of emerging infections. This perspective article describes how an emerging viral infection evolves from microbial mutation, zoonotic and/or vector-borne transmission that progresses to a fatal infection due to overt viremia, tissue-specific cytotropic damage or/and immunopathology. We classified immunopathogenesis of common emerging viral infections into 4 categories: 1) deficient immunity with disseminated viremia (e.g., Ebola); 2) pneumocytotropism with/without later hyperinflammation (e.g., COVID-19); 3) augmented immunopathology (e.g., Hanta); and 4) antibody-dependent enhancement of infection with altered immunity (e.g., Dengue). A practical guide to early blocking of viral evasion, limiting viral load and identifying the fatal mechanism of an emerging viral infection is provided to prevent and reduce the transmission, and to do rapid diagnoses followed by the early treatment of virus neutralization for reduction of morbidity and mortality of an emerging viral infection such as COVID-19.

Assessment of genetic diversity patterns of different serotypes of dengue virus, prevalent in patients from Kerala, India: a strain specific mutation study and its relevance to pathogenesis

“…However, tremendous efforts of the scientists to find out some antiviral therapy, there is no anti dengue drugs in the market presently. It is well known that; beneficial mutations generally map to intrinsically disordered domains of the virus which are clustered to a specific part in the genome [2; 49]. Several studies demonstrated that, the continuous influx of several mutations in the direction of virus adaptation [22; 40].…”

A compendium of multi-omics data illuminating host responses to lethal human virus infections

“…As such, they are classified as Category A (EBOV), B (WNV), or C (IAV and MERS-CoV) priority pathogens by the NIAID 1 . Host responses against all four viruses are thought to contribute to pathogenesis in severe and fatal cases 2 , 3 . Therefore, the overarching goal of the OMICS-LHV Systems Biology Center was to use global host response data to model virus infections and identify host-dependent mechanisms that regulate severe or fatal disease.…”

Hemorrhagic fever viruses: Pathogenesis, therapeutics, and emerging and re-emerging potential

“…Increased liberation of bradykinin, a potent inducer of vascular permeability, has also been reported in hantaviruses infections ( Taylor et al, 2013 ). In addition, the virion glycoprotein (GP) of the Ebola virus has been shown to mediate abnormal activation and disruption of endothelial cells even in the absence of viral replication ( Geisbert et al, 2003 ; Yang and Yang, 2021 ; Moni et al, 2022 ). Humans and nonhuman primates with VHF also present adrenocortical infection and necrosis, leading to impaired secretion of steroid-synthesizing enzymes that cause hypotension and sodium loss due to hypovolemia; these two important events have been reported in nearly all cases of VHF ( Mariappan et al, 2021 ).…”