Influenza Pandemics and Virus Infection Quiz

Influenza Pandemics and Virus Infection Process Summary

• The fatality rate for the pandemic was 0.13% of those infected, lower than the 1918 pandemic.
• The Asian Flu had a significant impact on public health despite a lower mortality rate.
• Historical pandemics highlight varying severity and impact of influenza strains on populations.
• New strains through antigenic shift and drift, lack of preexisting immunity can lead to large-scale outbreaks and high mortality rates.
• Efforts to prevent influenza pandemics include vaccine development, surveillance, and antiviral research.
• Viruses need to enter a host cell by binding to specific receptors and then penetrating or entering the cell.
• Uncoating exposes viral genetic material for replication inside the host cell.
• Viruses initiate early gene expression, often coding for proteins to evade host cell defenses and take control of the cell's machinery.
• Viruses employ strategies to evade the host cell's immune defenses and reprogram the host cell to support viral replication.
• Late viral gene expression is responsible for constructing new virions as the virus continues to replicate.
• Viral replication occurs within the host cell before the newly assembled virions are released through processes like budding or cell lysis.
• Released virions need to adhere to and infect new target cells to continue the infection cycle.

Title: Implications of Influenza Virus Rapid Mutations

• Rapid mutations lead to changes in viral surface proteins, reducing immune recognition and effectiveness of preexisting immunity.
• The need for frequent updates to influenza vaccines is a direct consequence of rapid mutations.
• The rapid mutation rate contributes to the seasonal variability of the flu, leading to variations in the severity of flu seasons.
• Antigenic drift allows the virus to escape the immune system's memory and cause recurrent infections in the same individuals.
• Influenza A's ability to undergo rapid antigenic drift and mutation can lead to the emergence of entirely new strains with pandemic potential.
• The constantly changing nature of the virus makes it challenging to predict vaccine efficacy, resulting in varying levels of effectiveness.
• Rapid mutations pose a significant challenge for individuals with compromised immune systems.
• Rapid mutations in influenza viruses exert selective pressure, favoring strains that can evade existing immunity.

Title: Implications of Influenza Virus Rapid Mutations and Antigenic Drift

• Influenza B primarily infects humans and causes seasonal epidemics due to its slower mutation rate.
• Influenza A can infect a wide variety of animals, including humans, has rapid mutation, and the potential to cause pandemics.

Influenza A Virus Antigenic Drift and Entry Mechanisms

• Influenza A viruses can infect a wide range of host species and have caused most influenza pandemics in history.
• Antigenic drift in influenza A viruses, particularly in the HA and NA genes, leads to the creation of new viral strains, necessitating updates to seasonal flu vaccines.
• Antigenic drift can result in changes in the hemagglutinin glycoprotein, particularly near the receptor-binding site, making the virus less recognizable to the immune system.
• The emergence of a new mutant form of hemagglutinin (HA), specifically the H1 subtype, in the 1918 Spanish Flu had a significant impact on the virulence of the virus.
• The lack of preexisting immunity to the new H1 subtype contributed to the rapid spread of the virus and increased severity of disease.
• The new H1 subtype may have undergone further mutations over time (antigenic drift), potentially altering the virus’s antigenic properties.
• Various mechanisms by which viruses can gain entry into host cells include pore-mediated penetration, endocytosis with dissolution of endosomal membrane, envelope fusion with plasma membrane, and endocytosis with fusion with endosomal membrane.
• Clathrin is a critical protein involved in clathrin-mediated endocytosis, a mechanism by which cells engulf molecules or particles from their external environment.
• Pore-mediated penetration involves the creation of pores in the host cell membrane through which the viral genome is injected, used by some human rhinoviruses and bacteriophages.
• Endocytosis involves the virus being engulfed by the host cell and forming an endosome, followed by dissolution of the endosomal membrane, used by adenoviruses.
• Envelope fusion with the plasma membrane allows certain viruses to enter the cell without being taken up into an endosome, employed by Morbilliviruses and Rubulaviruses.
• Endocytosis with fusion with the endosomal membrane allows some enveloped viruses to enter host cells through endocytosis, triggered by the low pH environment of the endosome, used by Herpes Simplex Virus and influenza viruses.