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In the 21st century, the rapidly changing global landscape have accelerated the emergence and spread of novel viral pathogens. Emerging zoonotic viral diseases pose a constant threat, and the appearance of a new virus or reemergence of a previously identified virus with diversified properties is cause for global concern. The current pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and other viral disease outbreaks, such as those of tick-borne SFTS and human infections with avian influenza viruses, serve as a constant reminder of how vulnerable humans are to emerging viral pathogens. The threat to public health posed by the emergence of novel fatal viral diseases has driven concentrated efforts to understand viral molecular and cellular biology. However, despite the attempts to elucidate the complexities of these emerging viruses, scant new information regarding the ever-changing threats posed by these viruses exists. This special issue provides a comprehensive review of emerging viral diseases. This information is an invaluable resource for those seeking to understand the mechanisms underlying host-virus interactions, which is necessary for controlling emerging fatal viral diseases, and provides insights into potential future pandemics.
Severe fever with thrombocytopenia syndrome (SFTS), a tick-borne infectious disease caused by a novel phlebovirus, is a growing global health concern. The main symptoms are high fever, low platelet and white blood cell levels, and gastrointestinal problems. The disease was first identified in China in 2009, and several SFTS epidemics have occurred in East Asia, with mortality rates of between 6 and 27 per cent. Researchers in South Korea led by Young Ki Choi at Chungbuk National University, Cheongju, review the latest research into SFTS virus and disease, including transmission, genetic diversity, epidemiology, pathology and clinical features, and pandemic potential. Animal models are helping researchers understand the virus and disease and develop treatments and vaccines.
Understanding how the innate immune system senses coronaviruses and how coronaviruses can escape detection could provide novel approaches to tackle infections. Coronaviruses, including SARS-CoV-2, constantly evolve to manipulate, obstruct and evade host immune responses. A team led by Ji-Seung Yoo, Hokkaido University, Sapporo, Japan, reviewed understanding of innate immune responses to coronaviruses and viral evasion strategies. Two major receptor families recognise RNA viruses upon infection, but how they respond to SARS-CoV-2 is unclear. One receptor, TLR7, plays a critical role in sensing coronavirus infections, and mutations in the TLR7 gene are associated with severe illness and mortality in young Covid-19 patients. Activating host TLR pathways may prove a useful therapeutic approach. Further in-depth investigations are needed into specific coronavirus proteins and viral mechanisms that suppress host immunity.
The long history of combating and planning for influenza pandemics should inform the fight against novel coronaviruses such as SARS-Cov-2. Richard Webby and co-workers at St. Jude Children’s Research Hospital in Memphis, USA review the history of preparing for influenza pandemics, including the global influenza surveillance network set up by the World Health Organization (WHO) in the 1950s. The 2009 H1N1 pandemic prompted WHO and the US Centers for Disease Control and Prevention to develop more detailed risk assessment tools drawing on laboratory research, genomics, industrial vaccine development, and surveillance of emerging animal strains that might transfer to humans. These tools and experience are proving successful in containing the H7N9 influenza that emerged in 2013, and could serve as models for managing coronaviruses, whose pandemic potential has only become apparent in the past two decades.
Extensive studies into how SARS-CoV-2 manipulates the immune system and influences the activity of host proteins are needed to improve treatments for COVID-19. SARS-CoV-2 evades or blocks elements of the immune system, including the antiviral activity of type I and type III interferons (IFN). You-Me Kim and Eui-Cheol Shin at the Korea Advanced Institute of Science and Technology, Daejeon, South Korea, reviewed understanding of how SARS-CoV-2 inhibits IFN responses. In infected cells, SARS-CoV-2 proteins use diverse methods to inhibit host IFN pathways, but type I IFN responses are still triggered in non-infected immune cells. The researchers believe this may explain the delayed but exaggerated type I IFN responses that contribute to the hyper-inflammation seen in critically ill patients. They call for further investigations into IFN and inflammatory responses in SARS-CoV-2 infection.