Influenza: Diagnosis, Treatment, Prevention - V.D. Moskalyuk 2010

Influenza
Origin of Epidemic Pathogens

Epidemic strains of Influenza A Viruses constantly replace one another. A new pathogen can trigger massive outbreaks across all age groups and countries, leading to a pandemic, or it may affect only a relatively small fraction of the population, causing an epidemic that flares up and quickly dies out. This behavior of the influenza virus is explained by The Structure of its surface envelope. Modern molecular biology techniques have made it possible to study all genes of human, animal, and avian influenza A viruses. It has been established that antigenic drift occurs due to the accumulation of so-called point Mutations—minute changes in The amino acid molecules of a Gene. During an epidemic, the population of circulating viruses consists of variants that differ precisely because of these mutations. A minor change in a tiny part of the antigen can render the virus immune to the neutralizing action of Antibodies, thereby causing disease. Consequently, point mutations in genes can be considered one of the primary evolutionary pathways of drift.

It is hypothesized that a complete alteration of one or both surface antigen genes, leading to The Emergence of an influenza pandemic, may result from genetic recombination (reassortment) between different human viruses, or possibly animal or avian ones. Some scientists believe that through recombination, the H2N2 virus emerged from the H1N1 virus, whereas H3N2 is a descendant of the H3N2 virus.

The high Variability of Influenza Viruses suggests that gene exchange between individual variants of virus A constantly occurs in nature. Although most subtypes of the influenza A virus are found in birds, their direct role in the emergence of new human influenza subtypes has not yet been proven.

Many questions remain unanswered for now. For instance, why does a new pathogen mostly emerge in China rather than anywhere else on Earth, why did older strains previously disappear upon its appearance, yet have not vanished since 1976? Where do they persist during the interepidemic period?

A partial answer to this question is provided by Kyiv virologist A.F. Frolov, who has been working on the influenza problem since the 1960s.

Experiments on Cells cultured in test tubes, and subsequently on animals, proved the incredible: the influenza virus is capable of residing within cells for a long time without destroying them. White mice that had survived influenza infection and recovered were re-examined 2 to 4 months later. Many of them had developed chronic Pneumonia. Using specially developed Methods, researchers successfully isolated the influenza virus 2, 4, 6 months, and even longer after the initial infection. Thus, the virus can live in the body for a long time and continuously maintain a disease state. Interestingly, the Organism does not actively react to the pathogen during this period; they interact without destroying each other.

This state is characteristic of many viruses and Bacteria and is known as persistence (constancy, preservation). The Discovery of the influenza virus's ability to persist prompted a team of scientists led by A.F. Frolov to explore a new hypothesis: the possibility of influenza virus persistence in the bodies of individuals who have recovered from the flu.

An attempt was made to isolate the influenza virus from a patient with pneumonia. The task was exceedingly difficult. Years passed, Research Methods and scientific approaches succeeded one another, but the desired results remained elusive. Finally, success arrived. Influenza viruses were isolated from patients suffering from chronic pneumonia and meningoencephalitis resulting from a previous bout of flu, proving that the viruses had been residing in The Human Body for a long time rather than accidentally entering it during or just prior to the examination.

These findings explained the cause of such severe influenza complications as pneumonia, Nervous system disorders, and others. The ROOT cause lies in the persistence of the pathogen.

Consequently, the influenza virus has no need to search for some reservoir or hiding place between epidemics where it can acquire new genes. The influenza pathogen can reside within us—in our own body cells—waiting for the right moment to attack. From time to time, it transitions into an active state, causing sporadic cases of illness and forming an epidemiological chain of small, isolated outbreaks.

During this period, Selection of the most aggressive pathogen variants takes place; the virus gradually gathers strength, infecting an increasingly larger number of susceptible individuals. And thus, an epidemic breaks out.

For now, this pathway of infection development remains a hypothesis, but scientists are comprehensively studying this possibility.

1. The Orthomyxoviridae family includes human, animal, and avian influenza viruses.

2. They possess an external envelope and contain single-stranded segmented RNA along with RNA polymerase.

3. The outer viral envelope consists of glycoprotein structures (hemagglutinin and neuraminidase) that determine its Specificity and The production of anti-influenza antibodies.

4. The most Characteristic Properties of orthomyxoviruses are:

5. The Genome consists of single-stranded fragmented RNA.

6. They do not replicate in the presence of actinomycin D and do not form infectious virions in enucleated cells.

7. They are distinguished by rapid antigenic variability, which leads to the emergence of new variants.