Influenza Virus: Transmission, Pathology, and Infection Control

Introduction to Influenza

Influenza ranks among the leading causes of death in the United States. It has been reported that the disease causes even greater harm in developing countries. During a flu epidemic, up to 20% of Americans are infected by the virus. Of this figure, approximately 36,000 people may die from the infection, and over 200,000 of those infected are hospitalized in facilities across the country. Indeed, few viruses have inflicted as much damage or endured as long as the influenza virus. Respiratory ailments attributed to influenza are documented in records tracing the infection back to ancient Greece and Rome. The word influenza, viewed in its original Greek form influentia, reflects the historical belief that epidemics were the result of the influence of the stars. Most people — including medical professionals — refer to influenza simply as the flu, yet many do not fully appreciate its distinct nature (Specter, 2005).

The cause of influenza is the Orthomyxovirus, which occurs in three forms termed A, B, and C. The B and C strains have the capacity to infect humans and make them ill, though these strains are comparatively rare and generally less serious when they do occur. It is Type A that presents the greatest concern. Each influenza virus carries hundreds of microscopic spikes that rise from its surface. These spikes are made of a protein called hemagglutinin, which allows the virus to latch onto and attach to cells it intends to infect. Another set of spikes consists of the enzyme neuraminidase, which provides the virus with much of its destructive power. These two proteins are the basis for naming flu virus subtypes, labeled by H type and N type. Type A influenza is known to be the most rapidly mutating form and thus the most successful at causing widespread damage. It can alter or swap any of its eight genes with those of variant strains (Specter, 2005).

The Nature of the Influenza Micro-Organism

The influenza genome is encased in a protein capsid. In influenza A, this capsid contains the antigenic glycoproteins neuraminidase (NA) and hemagglutinin (HA). Hundreds of molecules are required from each protein capsid. These are the portions of the virus recognized as foreign material by the host body's immune system. Because there are many varying types of influenza A neuraminidase and hemagglutinin proteins, the human immune system is frequently challenged in mounting an appropriate response. In addition to humans, other organisms are known to host and act as a reservoir for the influenza virus. Influenza outbreaks have been documented among poultry, pigs, camels, seals, and horses. When a strain is named, details of its origin, strain number, year of isolation, and NA/HA proteins are typically included (Clancy, 2008).

The influenza A genome has eight genes that encode 11 different types of proteins, including the NA and HA genes. The proteins include three RNA polymerases that work together in a complex arrangement needed to reproduce the viral RNA genome. Notably, these polymerases have a high error rate because they lack proofreading ability. This results in a high rate of mutation in replicated viral genomes and consequently a rapid rate of viral evolution. The influenza genome also encodes additional structural proteins required to form the capsid, the NS1 and NS2 proteins whose functions are still under investigation, and the nucleoprotein. Other proteins encoded by the genome include M1 and M2, which are needed for nuclear export and a range of other functions, as well as the NA and HA proteins that govern the attachment and release of the virus on host cells (Clancy, 2008).

Because the influenza genome is segmented — with coding sequences located within individual RNA strands — ready shuffling of genomes occurs within host cells when different flu virus strains are present simultaneously. Furthermore, given that there are at least 16 varying hemagglutinin subtypes and nine neuraminidase subtypes, a very large number of capsid protein combinations is possible. Of these subtypes, three hemagglutinin subtypes (H1 through H3) and two neuraminidase subtypes (N1 and N2) have driven sustained epidemics in the human population. All influenza A subtypes are known to circulate naturally in birds, which act as the reservoir from which HA subtypes can spread into the human population (Clancy, 2008).

Mode of Transmission

It is widely believed that influenza spreads through airborne means, whereby very small droplet nuclei containing the virus are inhaled, though direct evidence for this route remains limited. Theoretically, minute droplet nuclei leave the respiratory tract of infected individuals and, due to their small size and low mass, remain suspended in the air for a prolonged period. When inhaled by a new host, the virus enters the respiratory tract and attaches to specific receptor cells, or antigens, on the epithelial cell surface lining the trachea and pharynx. These infected cells replicate to produce a large mass of new viral particles, which then spread to infect additional body cells or leave the host to infect new victims.

Transmission of Type A influenza has been shown to be particularly rapid. The virus is also known to spread more quickly in enclosed spaces such as residential facilities, hospitals, and nursing homes. This observation has led to speculation that the virus may be spread during the prodromal stage, before symptoms become apparent in the infected individual. Studies have indicated that the virus can survive on stainless steel surfaces for up to eight hours and on tissue paper for only a few minutes (Gould, 2011).

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