Influenza A Pathophysiology and Clinical Manifestations

Introduction to Influenza A

The Centers for Disease Control and Prevention (CDC) notes that Influenza A is one of two types of influenza viruses that cause epidemic human disease, characterized by its unique viral structure and replication cycle, causing respiratory infection through antigenic drift and shift mechanisms 1, 2, 3

Influenza A viruses are categorized into subtypes based on two surface antigens: hemagglutinin (H) and neuraminidase (N), which are critical for viral attachment and release, according to the CDC 1, 2
The World Health Organization (WHO) reports that since 1977, influenza A (H1N1) and A (H3N2) have been the predominant subtypes in global circulation, with A (H1N2) variants emerging after genetic reassortment between human A (H3N2) and A (H1N1) viruses 4, 3

The CDC states that influenza A undergoes frequent antigenic changes through two primary mechanisms: antigenic drift, which involves point mutations during viral replication, and antigenic shift, which involves major changes in surface antigens through genetic reassortment between different influenza strains 1, 2, 3
Influenza A viruses undergo antigenic drift more rapidly than influenza B viruses, according to the CDC 1, 4

The CDC notes that the virus spreads primarily through respiratory droplets from coughing and sneezing of infected persons 1, 4
The incubation period ranges from 1-4 days, with an average of 2 days, as reported by the CDC 1

Uncomplicated influenza presents with abrupt onset of fever, myalgia, headache, malaise, nonproductive cough, sore throat, and rhinitis, according to the CDC 1, 4
Influenza can exacerbate underlying medical conditions, such as pulmonary or cardiac disease, as noted by the CDC 4, 6

The risk for complications, hospitalizations, and death is higher among persons aged >65 years, very young children, and individuals with underlying health conditions, according to the CDC 4, 6