SARS-CoV-2

The coronavirus SARS-CoV-2, which began spreading from Wuhan, China, in December 2019, is the causative agent of COVID19, a disease associated with severe acute respiratory syndrome (SARS). Within three months of its emergence, SARS-CoV-2 infected over 350,000 people globally, resulting in approximately 15,000 deaths. Before the SARS outbreak of 2002–2003 in Guangdong Province, China, coronaviruses were considered to cause primarily mild respiratory and intestinal infections. Ten years after SARS-CoV, another highly pathogenic coronavirus, MERS-CoV (*Middle East Respiratory Syndrome*), appeared in the Middle East. The natural reservoirs for SARS-CoV, MERS-CoV and SARS-CoV-2 are bats, which transmit the virus to humans via intermediate hosts, such as civets, camels and possibly pangolins. SARS-CoV-2 belongs to the beta-coronaviruses within the Coronaviridae family of the Nidovirales order. The virus enters human cells through a protein receptor called angiotensin-converting enzyme 2 (ACE2). ACE2 is critical for regulating blood pressure and heart rate and is present on cell surfaces in the lungs, heart, kidneys, and intestines. The virus binds to ACE-2 via its spike protein, a feature shared by related coronaviruses in bats, civets and pangolins. SARS-CoV-2 is encoded by a positive single-stranded RNA genome of about 30,000 nucleotides. Upon entering the host cell, the first step in its replication process is translating proteins necessary for viral particle formation, which includes the spike of envelope glycoprotein (S), envelope (E), membrane (M) and nucleocapsid protein (N), as well as proteins such as polymerase (Pol) and protease (Pr), which aid in virus multiplication but do not become part of the viral particle.