RNA viruses contain many essential and (re-)emerging human pathogens, such as HIV, Influenza, DENV, ZIKV, MERS-CoV, and the recently discovered SARS-CoV-2 which has caused the global outbreak of Coronavirus disease 2019 (COVID-19). Our immune system provides not only effective defense in the early phase but also specific long-term protection against invading viral infections through various mechanisms. For example, pattern recognition receptors (PRRs) mediated induction of interferon (IFN) response and subsequent IFN-stimulated genes (ISGs), pro-inflammatory cytokines, viral-specific cytotoxic T lymphocytes and neutralizing antibodies. However, many RNA viruses have developed multiple strategies to evade our immune system and establish productive or even persistent infection in host cells and tissues.
Investigations of immune evasion mechanisms developed by RNA viruses will help to understand the pathogenesis of viral infection and discover novel therapeutic targets for prevention and treatment of the diseases. Recently, Korber et al. found that D614G mutation increases the infectivity of SARS-CoV-2. Also, G614 is associated with a high level of viral nucleic acid in the human upper respiratory tract as well as high infectivity in multiple pseudotyping assays. These results suggested that the G614 variant may have a fitness advantage for SARS-CoV-2 replication in the upper respiratory tract. SARS-CoV-2 may cause lymphocytopenia through inducing T-cell apoptosis or autophagic cell death, which is similar to MERS-CoV. Several viral proteins of coronavirus can suppress type I IFN response and nuclear factor-?B signaling pathways, therefore facilitate innate immune evasion. Another important RNA virus, like HIV, has also evolved efficient strategies to counteract our immune surveillance and downregulate antiviral immune responses.
Despite the extensive studies carried out to better understand the immune evasion mechanisms by RNA viruses, there are still numerous questions that need to be addressed. Gaps still exist in many facets, including mechanisms of viral entry and replication at different cellular or tissue levels and their evolution/adaptation in different hosts. As RNA virus infection continues to cause a threat of global pandemics, we need to gain insight on interactions between viral infection and the immune responses and improve our understanding of host defenses. This knowledge will be crucial for the development of novel treatments and prevention strategies to limit the burden of human disease.
In this Research Topic, we will welcome the following manuscript types focusing on HIV, SARS-CoV-2, HCV or other RNA viruses and their immune evasion mechanisms.
Submissions are welcome for the following article types: Original Research, Brief Research Report, Reviews, Mini-Reviews, Systematic Reviews, Perspective, Opinion and hypothesis. Please note that abstract submission is not mandatory but encouraged, and you can submit your manuscript to the topic even without submitting an abstract. We particularly welcome contributions that include, but are not limited to, the following topics:
• HIV-/SARS-CoV-2-/HCV-/other RNA viral pathogenesis, and their immune evasion mechanisms.
• Immune responses in HIV-/SARS-CoV-2-/HCV-/other viral-infected patients.
• Role of interferons and inflammations in RNA virus pathogenesis.
• Viral-host interactions and how RNA viruses explore host mechanisms to evade the immune response.
• Clinical immunology of important viral diseases, including specific antibody and cellular immune responses to the viruses and the corresponding immune evasion by viruses.
• Mechanistic understanding of innate sensing of RNA viral infection in host cells and tissues.
• Discovery of novel prophylactic or therapeutic targets to overcome immune evasion by RNA viruses.
Therefore, unravelling novel molecular and immune virus evasion mechanisms will improve their prevention and control their infection.
RNA viruses contain many essential and (re-)emerging human pathogens, such as HIV, Influenza, DENV, ZIKV, MERS-CoV, and the recently discovered SARS-CoV-2 which has caused the global outbreak of Coronavirus disease 2019 (COVID-19). Our immune system provides not only effective defense in the early phase but also specific long-term protection against invading viral infections through various mechanisms. For example, pattern recognition receptors (PRRs) mediated induction of interferon (IFN) response and subsequent IFN-stimulated genes (ISGs), pro-inflammatory cytokines, viral-specific cytotoxic T lymphocytes and neutralizing antibodies. However, many RNA viruses have developed multiple strategies to evade our immune system and establish productive or even persistent infection in host cells and tissues.
Investigations of immune evasion mechanisms developed by RNA viruses will help to understand the pathogenesis of viral infection and discover novel therapeutic targets for prevention and treatment of the diseases. Recently, Korber et al. found that D614G mutation increases the infectivity of SARS-CoV-2. Also, G614 is associated with a high level of viral nucleic acid in the human upper respiratory tract as well as high infectivity in multiple pseudotyping assays. These results suggested that the G614 variant may have a fitness advantage for SARS-CoV-2 replication in the upper respiratory tract. SARS-CoV-2 may cause lymphocytopenia through inducing T-cell apoptosis or autophagic cell death, which is similar to MERS-CoV. Several viral proteins of coronavirus can suppress type I IFN response and nuclear factor-?B signaling pathways, therefore facilitate innate immune evasion. Another important RNA virus, like HIV, has also evolved efficient strategies to counteract our immune surveillance and downregulate antiviral immune responses.
Despite the extensive studies carried out to better understand the immune evasion mechanisms by RNA viruses, there are still numerous questions that need to be addressed. Gaps still exist in many facets, including mechanisms of viral entry and replication at different cellular or tissue levels and their evolution/adaptation in different hosts. As RNA virus infection continues to cause a threat of global pandemics, we need to gain insight on interactions between viral infection and the immune responses and improve our understanding of host defenses. This knowledge will be crucial for the development of novel treatments and prevention strategies to limit the burden of human disease.
In this Research Topic, we will welcome the following manuscript types focusing on HIV, SARS-CoV-2, HCV or other RNA viruses and their immune evasion mechanisms.
Submissions are welcome for the following article types: Original Research, Brief Research Report, Reviews, Mini-Reviews, Systematic Reviews, Perspective, Opinion and hypothesis. Please note that abstract submission is not mandatory but encouraged, and you can submit your manuscript to the topic even without submitting an abstract. We particularly welcome contributions that include, but are not limited to, the following topics:
• HIV-/SARS-CoV-2-/HCV-/other RNA viral pathogenesis, and their immune evasion mechanisms.
• Immune responses in HIV-/SARS-CoV-2-/HCV-/other viral-infected patients.
• Role of interferons and inflammations in RNA virus pathogenesis.
• Viral-host interactions and how RNA viruses explore host mechanisms to evade the immune response.
• Clinical immunology of important viral diseases, including specific antibody and cellular immune responses to the viruses and the corresponding immune evasion by viruses.
• Mechanistic understanding of innate sensing of RNA viral infection in host cells and tissues.
• Discovery of novel prophylactic or therapeutic targets to overcome immune evasion by RNA viruses.
Therefore, unravelling novel molecular and immune virus evasion mechanisms will improve their prevention and control their infection.
