Description, Causes, and Risk Factors:
The most common type of influenza. These strains have a high propensity for antigenic change resulting in mutations, partly because they can infect various animals where dual infections can occur, giving rise to new hybrid strains. The infections occur in epidemics, which may occur every 2-3 years and which vary in size and severity; perhaps the most important of the three types of influenza (A, B, and C).
Influenza A virus causes influenza in birds and some mammals, and is the only species of influenza virus A. Influenza virus A is a genus of the Orthomyxoviridae (The family of viruses that contains the 3 genera of influenza viruses, types A and B, C, and "Thogoto-like viruses." Virions are roughly spherical or filamentous, and the former (the more common form) are 80-120 mm in diameter and ether-sensitive; envelopes are studded with surface projections; nucleocapsids are of helical symmetry, 6-9 nm in diameter, and contain single-stranded, segmented RNA. The nucleoprotein antigen of each type of virus is common to all strains of the type but is distinct from those of the other types; the mosaic of surface antigens varies from strain to strain. Nucleocapsids seem to be formed in the nuclei of infected cells, hemagglutinin, and neuraminidase in the cytoplasm; virus maturation occurs during budding of the cell membrane. Influenza virus types A and B are subject to mutation resulting in epidemics. Influenza virus C differs from types A and B (e.g., lacks neuraminidase) and belongs to a separate genus) family of viruses. Strains of all subtypes of influenza A virus have been isolated from wild birds, although the disease is uncommon. Some isolates of influenza A virus cause severe disease both in domestic poultry and, rarely, in humans. Occasionally, viruses are transmitted from wild aquatic birds to domestic poultry, and this may cause an outbreak or give rise to human influenza pandemics.
Influenza A viruses are negative-sense, single-stranded, segmented RNA viruses. The several subtypes are labeled according to an H number (for the type of hemagglutinin) and an N number (for the type of neuraminidase). There are 17 different H antigens (H1 to H17) and 10 different N antigens (N1 to N10). The newest H antigen type, identified as H17 by researchers, was isolated from fruit bats in 2012.
Influenza type A viruses are categorized into subtypes based on the type of two proteins on the surface of the viral envelope:
H = hemagglutinin, a protein that causes red blood cells to agglutinate.
- N = neuraminidase, an enzyme that cleaves the glycosidic bonds of the monosaccharide, neuraminic acid.
Human infections with novel avian-origin influenza A (H7N9) virus were recently identified in March 2013, in China. As of May 17, a total of 131 human infections and 36 fatal cases have been reported. Nearly 84% of confirmed human cases (110 of 131) were from eastern China. The epidemiologic and virologic studies have revealed that poultry exposure may be an important risk factor for H7N9 infection in humans.
Severe disease in humans caused by a novel influenza A virus that is distinct from circulating human influenza A virus is a seminal event. It might herald sporadic human infections from an animal source — e.g., highly pathogenic avian influenza (HPAI) A (H5N1) virus; or it might signal the start of an influenza pandemic — e.g., influenza A (H1N1) virus. Therefore, the discovery of novel influenza A (H7N9) virus infections in three critically ill patients reported in the Journal of Medicine (JoM) is of major public health significance. US & Chinese scientists are to be congratulated for the apparent speed with which the H7N9 virus was identified, and whole viral genome sequences were made publicly available in relatively short period. Because this H7N9 virus has not been detected in humans or animals previously, the situation raises many urgent questions and Global public health concerns.
The hemagglutinin (HA) sequence data suggest that these H7N9 viruses are a low-pathogenic avian influenza (LPAI) A virus and that infection of wild birds and domestic poultry would, therefore, result in asymptomatic or mild avian disease, potentially leading to a "silent" widespread epizootic in China and neighboring countries. If H7N9 virus infection is primarily zoonotic, as reports currently suggest, transmission is expected to occur through exposure to clinically normal but infected poultry, in contrast to HPAI H5N1 virus infection, which typically causes rapid death in infected chickens.
The gene sequences also indicate that these viruses may be better adapted than other avian influenza viruses to infecting mammals. For example, the presence of Q226L in the HA protein has been associated with reduced binding to avian-like receptors bearing sialic acids linked to galactose by ?-2, 3 linkages found in the human lower respiratory tract (LRT), and potentially an enhanced ability to bind to mammalian-like receptors bearing sialic acids linked to galactose by ?-2, 6 linkages located in the human upper airway. Equally troubling is that Q226L in HA has been shown to be associated with transmission of HPAI H5N1 viruses by respiratory droplets in ferrets, one of the animal models for assessing pathogenicity and transmissibility of influenza viruses. These H7N9 viruses also possess the E627K substitution in the PB2 protein, which has also been associated with mammalian adaptation and respiratory-droplet transmission of HPAI H5N1 virus in ferrets. This H7N9 virus is a novel reassortant with HA and neuraminidase (NA) genes from an ancestral avian H7N9 virus and the six other genes from an avian H9N2 virus. The animal reservoir now appears to be birds, but many experts are asking whether these viruses might also be able to infect pigs, another common reservoir for zoonotic infections. The viral sequence data indicate antiviral resistance to the adamantanes and susceptibility to neuraminidase inhibitors, except for an R292K mutation in the NA protein of the A virus. Because this mutation has been associated with in vitro resistance to neuraminidase inhibitors in another N9 NA subtype virus, additional analyses must be undertaken to understand its significance. It is not known whether this mutation arises de novo in the host or is associated with treatment. Ongoing surveillance is crucial to assessing the emergence and prevalence of H7N9 viruses resistant to available antivirals.
Since available diagnostic assays used in clinical care (e.g., rapid influenza diagnostic tests) may lack sensitivity to identify H7N9 virus and since existing molecular assays will identify H7N9 virus as a unsubtypable influenza A virus, a critical public health issue is the rapid development, validation, and deployment of molecular diagnostic assays that can specifically detect H7N9 viral RNA. Such assays have been developed in China and are in development in many countries including the United States, and they will be deployed as they were for the 2009 H1N1 pandemic. Having available H7-specific assays will facilitate surveillance of H7N9 virus infections and help address key questions such as the duration of viral shedding, the infectious period, the optimal clinical specimens for laboratory confirmation, and the spectrum of clinical illness.
The clinical features described in the three patients with H7N9 virus infection, including fulminant pneumonia, respiratory failure, acute respiratory distress syndrome (ARDS), septic shock, multiorgan failure, rhabdomyolysis, and encephalopathy, are very troubling.
The key question for pandemic risk assessment is whether there is evidence of either limited or, more important, sustained human-to-human transmission — the latter being indicative of an emerging pandemic. If human-to-human transmission occurs, transmission dynamics, modes of transmission, basic reproductive number, and incubation period must all be determined. It is possible that these severely ill patients represent the tip of the iceberg and that there are much more as-yet-undetected mild and asymptomatic infections. Determining the spectrum of illness will help us understand the scope of the problem and assess severity. Enhanced surveillance for H7N9 virus infection is therefore urgently needed among hospitalized patients and outpatients of all ages with less severe respiratory illness. Other useful information can be derived from monitoring close contacts of patients with confirmed H7N9 cases to assess whether family members or health care personnel who provided care for patients with H7N9 virus infection have respiratory illness and laboratory-confirmed H7N9 virus infection. Such investigations will clarify whether H7N9 virus transmission in people appears efficient, or whether limited, non-sustained human-to-human transmission is occurring in persons with prolonged unprotected exposures, such as in clusters of HPAI H5N1 cases in blood-related family members. So far, the information provided by US & Chinese health officials provides reassurance that sustained human-to-human transmission is not occurring.
Clinical care of severely ill patients should be focused on evidence-based supportive management of complications such as ARDS. Adherence to recommended infection-control measures in clinical settings to reduce the risk of nosocomial transmission cannot be overemphasized.
All three patients with H7N9 virus infection reported by JoM (Journal of Medicine) received late treatment with Tamiflu™ starting on day 7 or 8 of illness while critically ill. Data related to human infections with seasonal, pandemic, and highly pathogenic avian influenza (HPAI) H5N1 viruses indicate that the earlier antiviral treatment is initiated, the greater the clinical benefit. Therefore, oral oseltamivir or inhaled Relenza® should be administered to patients with suspected or confirmed H7N9 virus infection as soon as possible. Secondary invasive bacterial infections associated with influenza can cause severe and fatal complications, and appropriate empirical antibiotic treatment for community-acquired bacterial infections may be indicated for initial management of severe H7N9 pneumonia. Caution should be exercised regarding the use of glucocorticoids, which are not indicated for the routine treatment of influenza. Clinical research, including randomized, controlled trials and observational studies, is urgently needed on new antiviral agents, including parenteral neuraminidase inhibitors and drugs with different mechanisms of action, combination antiviral treatment, and immunotherapy. To inform clinical management, rapid clinical data collection, data sharing, analysis, and timely feedback are needed worldwide.
NOTE: The above information is an educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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