The Seasonality of COVID-19
Reporter: Irina Robu, PhD
There are several similarities between SARS-CoV-2 and SARS-CoV, because both viruses share a high degree of homology to SARS-like coronaviruses isolated from bats. The entire genome of SARS-CoV-2 has 86% similarity with SARS-CoV. COVID-19, SARS-CoV-2 has a higher transmissibility than SARS-CoV, where more patients with COVID-19 have mild symptoms that contribute to spread because the patients are usually missed and not isolated.
Even in terms of disease dynamics, the similarities include transmission route via respiratory droplets. The angiotensin-converting enzyme 2 (ACE2), found in the lower respiratory tract of humans, has been identified as the receptor used for cell entry for both SARS-CoV and SARS-CoV-2.
So even though the viruses seem similar, there are some strong differences as well. Patients reports from China, Europe and United states show that some patients have also cardiac issues. The scientist do not truly understand what is happening at this point, whether people are having heart attacks (myocardial infarction) or whether the virus is actually invading the heart tissue to cause inflammation (myocarditis)
The great concern is that many people are asymptomatic with this condition, have no symptoms. This is what makes the virus so complicated is because you can have a group of patients severely sick and in the intensive care unit and in some cases, there are older individuals and some with underlying diabetes and heart disease, hypertension, renal disease.
Even though, the US has a large number of cases of over one million and at least 84,000 deaths, but due to undertesting, the true numbers of cases are probably far higher. The big unknown is that there is no clear understanding what is going to happen in the next coming months or years with the virus. However, the investigation models indicate that the virus has a probably of returning seasonally in the coming years.
Yet, people have to be mindful and recognize that even if we begin relaxing social distancing and transmission diminishes, that it could come back in these periodic waves, as suggested by the model.
SOURCE
https://www.medpagetoday.com/infectiousdisease/covid19/86049?xid=nl_mpt_DHE_2020-04-21
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This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.
This is very insightful. There is no doubt that there is the bias you refer to. 42 years ago, when I was postdocing in biochemistry/enzymology before completing my residency in pathology, I knew that there were very influential mambers of the faculty, who also had large programs, and attracted exceptional students. My mentor, it was said (although he was a great writer), could draft a project on toilet paper and call the NIH. It can’t be true, but it was a time in our history preceding a great explosion. It is bizarre for me to read now about eNOS and iNOS, and about CaMKII-á, â, ã, ä – isoenzymes. They were overlooked during the search for the genome, so intermediary metabolism took a back seat. But the work on protein conformation, and on the mechanism of action of enzymes and ligand and coenzyme was just out there, and became more important with the research on signaling pathways. The work on the mechanism of pyridine nucleotide isoenzymes preceded the work by Burton Sobel on the MB isoenzyme in heart. The Vietnam War cut into the funding, and it has actually declined linearly since.
A few years later, I was an Associate Professor at a new Medical School and I submitted a proposal that was reviewed by the Chairman of Pharmacology, who was a former Director of NSF. He thought it was good enough. I was a pathologist and it went to a Biochemistry Review Committee. It was approved, but not funded. The verdict was that I would not be able to carry out the studies needed, and they would have approached it differently. A thousand young investigators are out there now with similar letters. I was told that the Department Chairmen have to build up their faculty. It’s harder now than then. So I filed for and received 3 patents based on my work at the suggestion of my brother-in-law. When I took it to Boehringer-Mannheim, they were actually clueless.