We identified KLRD1-expressing NK cells as a potential biomarker for influenza susceptibility. Expression of KLRD1 was inversely correlated with symptom severity. Our results support a model where an early response by KLRD1-expressing NK cells may control influenza infection.
The NK cells are natural killer cells that help to control viral latency
This was reported as: Scientists discover biomarker for flu susceptibility
“We found that a type of immune cell called a natural killer cell was consistently low at baseline in individuals who got infected,” Bongen said. Those who had a higher proportion of natural killer cells had better immune defenses and fought off illness.
They have linked the virus-driven theft of quantized energy from the degradation of messenger RNA to differences in susceptibility to the influenza virus. They promote the use of ineffective vaccine by not telling anyone that one food energy-dependent RNA-mediated amino acid substitution makes the difference in whether the patient adapts or the virus adapts.
Khatri said his findings could help health professionals understand who’s at the highest risk for flu infection. “If, for example, there’s a flu epidemic going on, and Tamiflu supplies are limited, this data could help identify who should be prophylactically treated first,” Khatri said.
Health professionals already know who is at the highest risk for viral infections. These results could be used to establish pricing/availability to ensure that only the wealthy are protected during the forthcoming viral apocalypse.
Editor’s summary: Five antigenic sites in the virus surface hemagglutinin protein, which together comprise 131 amino acid positions, are thought to determine the full scope of antigenic drift of influenza A virus. Koel et al. (p. 976) show that major antigenic change can be caused by single amino acid substitutions. These single substitutions substantially skew the way the immune system “sees” the virus. All substitutions of importance are located next to the receptor-binding site in the hemagglutinin. Because there are few positions of importance for antigenic drift, there are strict biophysical limitations to the substitutions at these positions, which restricts the number of new antigenic drift variants at any point in time. Thus, the evolution of influenza virus may be more predictable than previously thought.
Viruses do not evolve. They adapt by stealing the quantized energy from cells that is required for cell types to establish viral latency. Energy-dependent microRNA-mediated multiple species re-assortment events link fixation of amino acid substitution in the host or in the virus to protection or susceptibility and pathogenicity.
Compared to the G2 RotaTeq vaccine strain, 17-24 amino acid changes, specifically A87T, D96N, S213D, and S242N substitutions in G2 epitopes, were observed.
These results suggest that the PA K338R mutation may be a molecular determinant of IBV pathogenicity via modulating the viral polymerase function of IBVs [Influenza B Viruses].
These 2018 HHMI Investigators are among others who are leading us towards the viral apocalypse via funding from HHMI.
Jesse Bloom Virus Evolution “I find it fascinating to watch evolution and see the amazing things that can occur by incremental small changes – where, in the end, the whole seems greater than its parts.”
Beth Shapiro Ancient DNA “What drives me is the abundance and diversity of life and the fear of running out of time. There is so much to learn. I want to be able to do it all.”
Howard Chang Gene Switches “I’m driven by the unexpected – the promise that there will be a unifying principle behind seemingly disparate facts.”
Feng Zhang Engineering Through Nature “I want to know how the world works, and to be able to do something that’s useful for people.”
Zhang adapted the CRISPR-Cas9 system and used it to edit DNA in mammalian cells.