COVID-19 and social distancing.

AIM: COVID-19 has spread rapidly worldwide since it began, greatly affecting peoples' lives, social economies and medical systems. At present, little is known about the disease, and vaccines are still under development. Therefore, in the face of severe outbreaks, previous effective experience can help people better protect themselves and their families. The aim of this article is to discuss the social distancing measures for COVID-19. SUBJECTS AND METHODS: Literature and document search. RESULTS: Recent research and a novel coronavirus pneumonia prediction model revealed social distancing measures and wearing masks are required to mitigate hospital system overload and prevent pathogen exposure. After a series of social distancing measures, there are 309 cities with zero cases and 34 cities with confirmed cases in China as of April 13, 2020. CONCLUSION: From China's experience with novel coronavirus pneumonia, we know that social distancing is the most effective measure at present. We need to win more time to allow limited medical resources to save lives.

COVID-19 and social distancing

Aim: COVID-19 has spread rapidly worldwide since it began, greatly affecting peoples' lives, social economies and medical systems. At present, little is known about the disease, and vaccines are still under development. Therefore, in the face of severe outbreaks, previous effective experience can help people better protect themselves and their families. The aim of this article is to discuss the social distancing measures for COVID-19. Subjects and methods: Literature and document search. Results: Recent research and a novel coronavirus pneumonia prediction model revealed social distancing measures and wearing masks are required to mitigate hospital system overload and prevent pathogen exposure. After a series of social distancing measures, there are 309 cities with zero cases and 34 cities with confirmed cases in China as of April 13, 2020. Conclusion: From China's experience with novel coronavirus pneumonia, we know that social distancing is the most effective measure at present. We need to win more time to allow limited medical resources to save lives.

CD147 antibody specifically and effectively inhibits infection and cytokine storm of SARS-CoV-2 and its variants delta, alpha, beta, and gamma.

SARS-CoV-2 mutations contribute to increased viral transmissibility and immune escape, compromising the effectiveness of existing vaccines and neutralizing antibodies. An in-depth investigation on COVID-19 pathogenesis is urgently needed to develop a strategy against SARS-CoV-2 variants. Here, we identified CD147 as a universal receptor for SARS-CoV-2 and its variants. Meanwhile, Meplazeumab, a humanized anti-CD147 antibody, could block cellular entry of SARS-CoV-2 and its variants-alpha, beta, gamma, and delta, with inhibition rates of 68.7, 75.7, 52.1, 52.1, and 62.3% at 60 µg/ml, respectively. Furthermore, humanized CD147 transgenic mice were susceptible to SARS-CoV-2 and its two variants, alpha and beta. When infected, these mice developed exudative alveolar pneumonia, featured by immune responses involving alveoli-infiltrated macrophages, neutrophils, and lymphocytes and activation of IL-17 signaling pathway. Mechanistically, we proposed that severe COVID-19-related cytokine storm is induced by a "spike protein-CD147-CyPA signaling axis": Infection of SARS-CoV-2 through CD147 initiated the JAK-STAT pathway, which further induced expression of cyclophilin A (CyPA); CyPA reciprocally bound to CD147 and triggered MAPK pathway. Consequently, the MAPK pathway regulated the expression of cytokines and chemokines, which promoted the development of cytokine storm. Importantly, Meplazumab could effectively inhibit viral entry and inflammation caused by SARS-CoV-2 and its variants. Therefore, our findings provided a new perspective for severe COVID-19-related pathogenesis. Furthermore, the validated universal receptor for SARS-CoV-2 and its variants can be targeted for COVID-19 treatment.

CD147-spike protein is a novel route for SARS-CoV-2 infection to host cells.

In face of the everlasting battle toward COVID-19 and the rapid evolution of SARS-CoV-2, no specific and effective drugs for treating this disease have been reported until today. Angiotensin-converting enzyme 2 (ACE2), a receptor of SARS-CoV-2, mediates the virus infection by binding to spike protein. Although ACE2 is expressed in the lung, kidney, and intestine, its expressing levels are rather low, especially in the lung. Considering the great infectivity of COVID-19, we speculate that SARS-CoV-2 may depend on other routes to facilitate its infection. Here, we first discover an interaction between host cell receptor CD147 and SARS-CoV-2 spike protein. The loss of CD147 or blocking CD147 in Vero E6 and BEAS-2B cell lines by anti-CD147 antibody, Meplazumab, inhibits SARS-CoV-2 amplification. Expression of human CD147 allows virus entry into non-susceptible BHK-21 cells, which can be neutralized by CD147 extracellular fragment. Viral loads are detectable in the lungs of human CD147 (hCD147) mice infected with SARS-CoV-2, but not in those of virus-infected wild type mice. Interestingly, virions are observed in lymphocytes of lung tissue from a COVID-19 patient. Human T cells with a property of ACE2 natural deficiency can be infected with SARS-CoV-2 pseudovirus in a dose-dependent manner, which is specifically inhibited by Meplazumab. Furthermore, CD147 mediates virus entering host cells by endocytosis. Together, our study reveals a novel virus entry route, CD147-spike protein, which provides an important target for developing specific and effective drug against COVID-19.