Random variation is an essential component of all living things. It encourages diversity, and that’s why there are so many different species. Viruses are no exception. Most viruses are experts at changing the genome to adapt to their environment. We now have evidence that the virus that causes Covid, SARS-CoV-2, is not only changing but also significant. This is the twenty-fourth in a series of articles on how viruses change and what they mean for humanity. Read the rest: part one, The second part, Third part, part four, part five, section six, section seven, section eight, section nine, section ten, section eleven, part twelve, section thirteen, section fourteen, section fifteen, section sixteen, section seventeen, section eighteen, section nineteen, section twenty, section twenty one, part twenty two, and section twenty three.
When the SARS-CoV-2 variants developed mutations, they increased their ability to spread, make sick, and fight antibodies, resulting in more tougher cases of Covid-19. Earlier this month, I detailed one of the variants that started circulating in Southern California (B.1.427 / 429). In the weeks since then, the spread of the virus has been predictable, and the most recent data describing its structure and spread echoes the dangers I fear transmit to people in California, the United States, and the world at large.
To refresh, the viral strain was first described by a genome sequencing attempt from Cedars Sinai Hospital in Los Angeles. From their variant surveillance efforts, they have been tracking the dangerous strain of SARS-CoV-2 since July 2020. In the months since then, B.1.427 / 429 has spread among the population to more than half of the isolates analyzed in California in recent times . January. We postulated that their different mutations – S13I, W152C, and L452R – would result in higher transmissibility and increased antibody resistance, similar to the strains of Great Britain, South Africa and Brazil. This mutation and other mutations are depicted in the image below. I am talking in more detail about individual mutations and their functions here.
Looks like our fears are manifested. New data announced by Dr. Charles Chiu of the University of California San Francisco demonstrates B.1.427 / 429’s destructive abilities in detail. The study, according to Chiu, will be published in the future day. Samples collected from a number of California states showed 19 to 24% more variants were transmissible. One elderly care facility experienced an almost six-fold increase in transmission from the previous virus.
In addition, it appears that viral load has also increased among patients. Compared with individuals infected with the non-B.1.427 / 429 version of the virus, those infected with the California variant were measured viral load about twice as high. A greater viral load has some dire implications. First, people who are infected are much more likely to experience severe symptoms or symptoms in general. Second, they may have a longer duration of infection, shown in a study of a group of NBA basketball players player. Third, they have a greater chance of infecting other people, because every sneeze, cough and breath carries a larger proportion of virus particles.
As expected, the mutation in B.1.427 / 429 conferred a significant level of antibody resistance, both for natural antibodies from previous infection, and those given by vaccination. Much of this can be attributed to the L452R mutation alone, which is located in the receptor-binding domain: the mechanism that connects to the ACE2 receptor in human cells. One version of the virus called CAL.20A which only underwent this mutation saw an infectivity rate that was 40% higher than the common B.1.427 / 429 strain and 200% higher than the initial wild-type virus in the cohort. gorilla at the San Diego Zoo.
Further research from the San Francisco study showed increased virulence as well. In line with observed increases in viral load, the investigators found a 21% increase in ICU admissions and an eleven-fold increase in mortality among those infected with B.1.427 / 429.
However, spike protein may not be the only source of this embarrassing data. Various mutations outside of the spike protein can lead to increased immune escape, transmission, and virulence as well. Among these mutations are the T114I and S385T point mutations in non-structural protein 4, which is a transmembrane protein. Changes to this mechanism can increase immune escape, which this breed exhibits. Mutation of P323L into non-structural protein 12, which is present in many strains such as the UK, South Africa, Brazil and many more in the US, is involved in transcription. Mutations in this mechanism are likely to increase viral load resulting in transmission and virulence. The various mutations outside the spike protein are depicted in the image below.
These numbers are staggering. They describe the full power of the variant. In a matter of months, B.1.427 / 429 grew from one isolate to more than half the cases in the state. Undoubtedly, this variant has spread along the Pacific coast to the continental United States. We find ourselves in battle against an emerging horde of strains, all equipped with advanced weaponry: immune escapes, increased virulence and greater contagion. We have to upgrade our tools too with stronger public health efforts, variant surveillance, and maybe an adaptive vaccine if we are to win this war.