Covit 19

Pujarchana Mohanty 0 Comments 4 May, 2020 18:45

COVID-19 Vaccine Will Close in on the Spikes, As epidemiologists try to stay ahead of the spread of new coronavirus COVID-19, vaccine developers, like Sanofi and Johnson & Johnson, are focusing on the “spike” proteins that festoon viral surfaces. Following clues in genomes is critical to disrupting the tango of infectivity as viruses meet and merge with our cells. Vaccine developers look specifically to the molecular landscapes where viruses impinge upon our respiratory and immune system cells. Targeting COVID-19 is especially challenging, because efforts to develop a vaccine against its relative, the SARS coronavirus (SARS-CoV), elicit only partial responses. But those steps are now serving as jumping off points for pharma. The relationship between viruses and humans can seem like a science fiction plot. The viruses that make us sick may be little more than snippets of genetic material borrowed, long ago, from human genomes. Packaged with their own proteins, viruses return to our bodies, taking over to make more of themselves.A zoo of animal hosts Coronaviruses present a “severe global health threat,” write researchers from Wuhan University and Sun Yat-sen University in the Journal of Medical Virology. The viruses aren’t new, nor do they infect only people. They cause: diarrhea in pigs, dogs, and cows fever and vasculitis in cats fever and anorexia in horses severe lung injury in mice lung disease and death from liver failure in whales respiratory tract infection in birds (bulbuls, sparrows, and chickens) Bats’ immune response enables them to house coronaviruses without becoming sick, making them a dangerous reservoir of infection. Some species spread coronaviruses without becoming sick, like the camels that carry MERS, and bats, which carry many viruses. Human Coronaviruses Before COVID-19 Before December 2019, six coronaviruses were known to infect humans. The first two, HCoV-229E and HCoV-OC43, were discovered in the 1960s.

A zoo of animal hosts Coronaviruses present a “severe global health threat,” write researchers from Wuhan University and Sun Yat-sen University in the Journal of Medical Virology. The viruses aren’t new, nor do they infect only people. They cause: diarrhea in pigs, dogs, and cows fever and vasculitis in cats fever and anorexia in horses severe lung injury in mice lung disease and death from liver failure in whales respiratory tract infection in birds (bulbuls, sparrows, and chickens) Bats’ immune response enables them to house coronaviruses without becoming sick, making them a dangerous reservoir of infection. Some species spread coronaviruses without becoming sick, like the camels that carry MERS, and bats, which carry many viruses. Human Coronaviruses Before COVID-19 Before December 2019, six coronaviruses were known to infect humans. The first two, HCoV-229E and HCoV-OC43, were discovered in the 1960s. They cause about 30% of colds, with rare case reports of pneumonia in patients who had other viral infections or were immunocompromised. In 2002 came SARS-CoV and in 2004 HCoV-NL63, which causes pneumonia and bronchitis, rarely. SARS (severe acute respiratory syndrome) caused more than 8,000 infections and 774 deaths, but most of us have antibodies to NL63, indicating past exposure that didn’t make us very sick. In 2005 came HKU1. It causes pneumonia in young children and 1.5% of cases of adult respiratory distress syndrome. MERS-CoV (Middle Eastern Respiratory Syndrome) emerged in 2012 in the Arabian peninsula, and is rare but can be fatal. SARS and MERS show zoonotic (to other animals) as well as human-to-human transmission. Two coronaviruses without a predilection for human bodies may also be important, epidemiologically speaking. HKU2, which killed 24,000 piglets in southern China from diarrhea in 2017, is the first “spillover” from a bat coronavirus to livestock. And Beluga whale CoV/SW1, although only distantly

COVID-19 latches onto angiotensin-converting enzyme 2, aka ACE2. To us, ACE2 is an enzyme that has an effect on blood pressure. To COVID-19, ACE is a receptor, an entranceway, in the airways and alveoli (air sacs) as well as in blood vessel linings. ACE is also a receptor for SARS-CoV and NL63-CoV. (MERS-CoV uses a different receptor.) The key to developing vaccines and treatments is the three-dimensional shapes of the parts of the virus that contact our cells. SARS and NL63-CoV bind to a helical part of ACE2 that snakes up from cell membranes, forming distinctive tunnels and bridges that comprise a “hot spot” for viruses. The attraction of a virus to a cell receptor hot spot is a little like a tired commuter emerging from a subway station and seeing a Starbucks sign, moving towards the coffee shop as if dragged by a tractor beam. The viral hot spot that beckons both SARS and COVID-19 is a shared drug and vaccine target – and so all the work on developing a SARS vaccine is now in the spotlight. Researchers knew from SARS that the S1 parts of the viral spikes hug the ACE receptor at a region of five amino acids (protein building blocks). Even though four of the amino acids differ in COVID-19, they are similar in size and charge to their counterparts in SARS. If S1 attaches SARS to the ACE receptor like a boat docking, would COVID-9 tie up at exactly the same points? Teaming a traditional crystal structure approach with computational methods, Pei Hao, of the Chinese Academy of Sciences and colleagues modeled the interface, showing that COVID-19 indeed binds ACE2 just like SARS does, with slightly less force. In a Letter to the Editor of Science China Life Sciences, they conclude that the new virus “poses a significant public health risk for human transmission via the S-protein-ACE binding pathway.” Even more recently, researchers from the University of Texas at Austin and the National Institute of Allergy and Infectious Disease used

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