A tug-of-war between severe acute respiratory syndrome coronavirus 2 and host antiviral defence: lessons from other pathogenic viruses

Abstract

World Health Organization has declared the ongoing outbreak of coronavirus disease 2019 a Public Health Emergency of International Concern. The virus was named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the International Committee on Taxonomy of Viruses. Human infection with SARS-CoV-2 leads to a wide range of clinical manifestations ranging from asymptomatic, mild, moderate to severe. The severe cases present with pneumonia, which can progress to acute respiratory distress syndrome. The outbreak provides an opportunity for real-time tracking of an animal coronavirus that has just crossed species barrier to infect humans. The outcome of SARS-CoV-2 infection is largely determined by virus-host interaction. Here, we review the discovery, zoonotic origin, animal hosts, transmissibility and pathogenicity of SARS-CoV-2 in relation to its interplay with host antiviral defense. A comparison with SARS-CoV, Middle East respiratory syndrome coronavirus, community-acquired human coronaviruses and other pathogenic viruses including human immunodeficiency viruses is made. We summarize current understanding of the induction of a proinflammatory cytokine storm by other highly pathogenic human coronaviruses, their adaptation to humans and their usurpation of the cell death programmes. Important questions concerning the interaction between SARS-CoV-2 and host antiviral defence, including asymptomatic and presymptomatic virus shedding, are also discussed. ARTICLE HISTORY

Harnessing innate immunity to eliminate SARS-CoV-2 and ameliorate COVID-19 disease

“…Hypothetically, it is plausible that elevated neutrophil abundance is associated with increased reactive oxygen species (ROS) and neutrophil extracellular traps (NETs), both of which are potent antimicrobial defenses; yet inappropriate levels of these neutrophil-derived products can inflict tissue damage. This tissue damage could contribute to a "proinflammatory cytokine storm" initiated by macrophages and monocytes infiltrating the damaged tissue (15,23,37). This inflammatory response occurring at a late stage of infection can cause aggravated respiratory/cardiovascular problems.…”

Managing Cutaneous Immune-Mediated Diseases During the COVID-19 Pandemic

“…Highly pathogenic human CoV infections suppress type I interferon (IFN) production and signaling, the key component of host antiviral defense in the early phase of viral replication, thus exacerbating disease progression [5]. In line with SARS and MERS, SARS-CoV-2 infection in severe cases involves the host response as an important contributor to the disease process and tissue damage, mainly due to dysregulated and excessive innate immune responses.…”

The unsynchronized changes of CT image and nucleic acid detection in COVID-19: reports the two cases from Gansu, China

“…When SARS-CoV-2 enters humans, the interplay between virus and host antiviral defence is a governed factor for outcome of infection. Asymptomatic carriers might arise when host antiviral defence is either strong or decoupled, thus asymptomatic shedding might occur when the immune response effectively limits but could not enough to completely block SARS-CoV-2 replication [6]. Thus, the continued treatment and isolated is needed, since the risk of transmitting to others still exist.…”