The pathophysiology of SARS-CoV-2 infection closely resembles that of SARS-CoV infection, with aggressive inflammatory responses strongly implicated in the resulting damage to the airways 21. Severe COVID-19 cases progress to acute respiratory distress syndrome (ARDS), on average around 8–9 days after symptom onset 11, 20. Within 5–6 days of symptom onset, SARS-CoV-2 viral load reaches its peak - significantly earlier than that of the related SARS-CoV, where viral load peaks at about 10 days after symptom onset 16, 17, 18, 19. At the point of hospital admission, patients with COVID-19 typically exhibit a fever and dry cough less commonly, patients also experience difficulty in breathing, muscle and/or joint pain, headache/dizziness, diarrhoea, nausea and the coughing up of blood 6, 10, 11, 12, 13, 14, 15. On infection, the median incubation period is approximately 4–5 days before symptom onset 6, 7, 8, 9, with 97.5% of symptomatic patients developing symptoms within 11.5 days 8. Like the other respiratory coronaviruses, SARS-CoV-2 is transmitted primarily via respiratory droplets, with a possible, but unproven, faecal–oral transmission route. However, among all known coronavirus sequences, SARS-CoV-2 is most similar to bat coronavirus RaTG13, with 98% similarity 4, and coronavirus sequences in the pangolin (a scaly anteater) also share high similarity 5. Its closest relative among human coronaviruses is SARS-CoV, with 79% genetic similarity 3.
SARS-CoV-2 belongs to the betacoronavirus genus. However, there are three coronaviruses (severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV) and SARS-CoV-2) that can replicate in the lower respiratory tract and cause pneumonia, which can be fatal. Among these, four (human coronaviruses 229E, NL63, OC43 and HKU1) typically infect only the upper respiratory tract and cause relatively minor symptoms 2. Moreover, we discuss how studies focused on the adaptive immune response will be crucial in informing the development of vaccines and therapeutic monoclonal antibodies.Ĭoronaviruses are known to cause disease in humans and animals. Specifically, we highlight the implications of specific features of the infection for promising therapeutic interventions that could target the virus or the dysfunctional immune response. Here, we review the literature on SARS-CoV-2 pathophysiology, its interaction with target cells and the immune response to the virus, including the contribution of dysfunctional immune responses to disease progression. Therefore, there is an urgent need to better understand the host–pathogen biology of COVID-19 as this will offer important insights into treatment and management of the disease, including identification of new therapies. Daily reports of sharp rises in the number of new cases continue to emerge from many countries/regions, but efforts to overcome the virus are hampered by a lack of knowledge of several important aspects of SARS-CoV-2 infection, ranging from pathogen biology to host response and treatment options. By 24 March 2020, SARS-CoV-2 had infected more than 381,000 people across 195 countries/regions and killed more than 16,000: a pandemic as declared by the World Health Organization 1. The causative virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is capable of human-to-human transmission and spread rapidly to other parts of China and then to other locations. The first cases of coronavirus disease 2019 (COVID-19) likely occurred from a zoonotic transmission in China in December 2019, linked to a large seafood market that also traded in live wild animals. Finally, we highlight the implications of these approaches for potential therapeutic interventions that target viral infection and/or immunoregulation. From nascent reports describing SARS-CoV-2, we make inferences on the basis of the parallel pathophysiological and immunological features of the other human coronaviruses targeting the lower respiratory tract - severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). We describe the interaction of SARS-CoV-2 with the immune system and the subsequent contribution of dysfunctional immune responses to disease progression. Here, we provide an overview of the pathophysiology of SARS-CoV-2 infection. Alongside investigations into the virology of SARS-CoV-2, understanding the fundamental physiological and immunological processes underlying the clinical manifestations of COVID-19 is vital for the identification and rational design of effective therapies. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the ongoing coronavirus disease 2019 (COVID-19) pandemic.
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