Virology and Scientific Advances

In the early stages of the pandemic, a few variants of concern easily gained an evolutionary advantage and spread easily around the world. When variants such as Alpha, Delta emerged, they easily spread around the world. One variant easily outperformed the other variant in a population and caused a new wave of Covid. However, Beta and Gamma variants could not spread to the whole world due to the faster transmission of the Alpha variant. The Alpha variant was destroyed by the Delta variant.   But after Omicron, the number of variants of concern started to increase. Most of these variants are very contagious; we are now watching the evolutionary race of different variants. BA.1.1, BA.2, BA.2.2, BA.2.8 and now BA.2.12.1, BA.4 and BA.5. BA.2.2 had a chance to spread in Hong Kong, BA.2 had a chance to spread in England, and BA.2.8 had a chance to spread in Scotland; and then serious waves were seen around here. For a variant to cause a surge in a population, it must first tak

Covid-19 is not just a lung-damaging disease. Covid-19 damages many organs and systems.  We must take precaution against Covid-19 for humanity. The incidence of Long Covid in Covid cases is 40% for some symptoms, 30% for some symptoms, 20% etc. The world is facing a virus that leaves its Long Covid sequelae and most likely infects T-lymphocytes. The increased ACE2 affinity after the Omicron variant of SARS-CoV-2, its ability to infect cells by endosomal way, show us the risk of increasing Long Covid cases. It has been 3-5 months since the Omicron BA.1 and BA.2 outbreaks. And at this point, Long Covid cases have increased a lot and caused a human tragedy. There are so many people suffering from Long Covid sequelae that the number of people who can work as an economic workforce is decreasing. The newly identified variants of concern BA.2.12.1, BA.4 and BA.5 are spreading rapidly all over the world. There may be new pandemic waves originating from these variants in the coming period. We m

 Pox viruses are DNA viruses. Monkeypox virus is among the Orthopoxviruses that have the ability to infect humans, including the Variola virus. The virus contains a lipoprotein membrane on the outside. There are proteins on this membrane that play a role in virulence and entry into the cell. The genome of the virus consists of three regions. The genome center contains genes involved in viral replication. The terminal region of the genome is responsible for the virus host and inflammation. At the far end of the genome are the genes that join the DNA ends of the virus. Monkeypox virus is an old virus. The natural host of the Monkeypox virus is squirrels. The virus is transmitted to humans through animal contact, and there is human-to-human transmission. So far, only sporadic cases have been seen because of this. However, in recent days, the cases that seem to be independent of each other and that have appeared one after another in different countries, "Has the virus's ability to

Omicron is the variant with the best S1-S2 cleavage ability by the human protease furin. The spike protein of the Omicron variant is in the open conformation. The spike protein of the original virus had almost completely closed and loose conformation. In the original virus, the S1-S2 regions on the spike are mixed and loosely connected to each other. Due to mutations, S1 subunits and neighboring S2 regions are more tightly packed together in Omicron. This is why Omicron's spike protein is stronger, more stable and capable of better ACE II affinity than previous variants.   In the evolutionary history of SARS-CoV-2, we have seen more infectious variants arise. Mutations such as D614G, N501Y have made the spike protein more open. This may result in more RBD regions being exposed and this may mean that the virus has better receptor binding and tends to be more contagious. More than 1 million variants of SARS-CoV-2 have emerged. However, since most of these contain mutation

 Long Covid and Omicron SARS-CoV-2 can spread from cell to cell through cell walls. This is a way of hiding from the immune system. This ability was limited in SARS-CoV-1. SARS-CoV-1 leaves the infected cell and infects new cells through receptors. This is the classic way. This leaves the virus more vulnerable to immune system attacks and antibody neutralization. This feature of SARS-CoV-2 is very important in terms of hiding it from the immune response..  Variants from SARS-CoV-2 and SARS-CoV-2 use ACE2 and TMPRSS2 receptors to infect cells. However, with the Omicron BA.1, this situation has changed. TMPRSS2 is an abundant receptor in the lung. Omicron has a lower affinity for the TMPRSS2 receptor than other variants.( 5 times less than Delta). This explains why Omicron BA.1 has less lung pathogenicity than Delta.  In addition, Omicron can enter the cell directly by the endosomal route without ACE2 and TMPRSS2. This ability was almost non-existent in previous variants.  And Omicro