Antiviral Therapy in Patients With Influenza

Marie Welch, PharmD; Casey Mabus, PharmD; John A. (Jake) Galdo, PharmD, BCPS, BCGP

Disclosures

US Pharmacist. 2017;42(4):32-36. 

In This Article

Pathophysiology

Influenza A and B have similar structures: a negative-strand RNA consisting of eight gene segments encapsulated and covered by the proteins hemagglutinin (HA), neuraminidase (NA), and matrix 2.[1] The HA protein recognizes and attaches itself to a host cell, where the virus RNA traps itself in an endosome, releasing its viral particles into the nucleus of the host cell for replication.[5,6] The influenza A virus first replicates in the nasopharynx and eventually moves replication to the upper and lower respiratory tracts. Infected individuals are contagious for up to a week after symptoms occur; this is because viral replication declines slowly and the virus is shed at least 7 days after illness.[1,7]

Influenza A is divided into two subgroups based on HA and NA surface proteins. There are 18 different HA proteins and 11 NA proteins, and each influenza A virus consists of one HA surface protein and one NA surface protein.[8] The different HA and NA proteins and their combinations are from viral mutations occurring during the replication process by two different mechanisms.[8]

First, an antigenic drift can occur in which the virus creates small genetic changes during replication. These changes create a virus that is highly similar to its original, since both share the same antigenic properties. Over time, the changes render the virus unrecognizable to human antibodies.[9] The second mechanism, known as antigenic shift, causes a pronounced alteration in the influenza A virus.[9] The new virus has different antigenic properties and different HA and/or NA proteins.[9] Antigenic shift is one of the reasons for the 2009 influenza pandemic.[9]

After infection, the immune system creates antibodies against the HA and NA surface proteins of the specific virus.[1] A vaccine of the attenuated or live virus is introduced into the body for the production of antibodies against the influenza antigens.[10,11] The antigenic shift and drift to the RNA virus render the development of the influenza vaccine prognostic.[10] Therefore, researchers use data collected from previous years and trends to determine which three or four viral strains should constitute the vaccine's composition.[11,12]

The CDC developed a surveillance system to track the progression of the influenza virus each year to aid in vaccine development. Data collected include the location and timing of the viral activity, influenza types and subtypes, any antigenic changes or mutations, reports of influenza-like illnesses, influenza-related hospitalizations, and influenza-related deaths.[13] For the 2016–2017 season, influenza A (H3N2) has been reported most commonly, followed by influenza A (H1N1pdm09); however, some influenza B types have also been reported.[3]

Vaccination is an effective measure of prevention against the influenza virus, having 70% to 90% efficacy against influenza A.[1] However, with the continuous small changes caused by antigenic drift, a vaccinated person still could become infected with the influenza virus, and treatment may be deemed appropriate.[9]

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