Influenza, a respiratory infectious disease caused by influenza viruses, typically peaks in incidence during autumn and winter. It spreads through respiratory droplets and triggers a systemic inflammatory and immune responses during infection, leading to symptoms such as fever, headache, and muscle soreness.
Influenza viruses are highly mutable. Based on differences in their nucleoprotein and matrix protein, influenza viruses are classified into four types: A, B, C, and D. Influenza C virus (ICV) is a lesser known type of influenza virus. ICV is usually associated with mild respiratory disease. The most common symptoms of ICV infection are fever, rhinorrhea, and cough; however, the virus has been associated with pneumonia, bronchiolitis, and bronchitis[1, 2]. Additionally, symptoms of gastroenteritis in patients infected with ICV are frequently reported.
ICV is mainly a human pathogen; however, the virus has been detected in pigs, dogs, and cattle, with rare cases of swine-human transmission reported[3, 4]. Although ICV was discovered in 1947, its disease burden was poorly described until recently due to the difficulty in isolating the virus in cell culture[5, 6]. Seasonality of ICV is poorly understood, although outbreaks and cases of familial transmission have been described[7].
ICV is an enveloped, negative-sense RNA virus that belongs to the Orthomyxoviridae family. It has a 7-segmented genome that encodes 9 viral proteins[8]. Influenza A and B surface proteins include hemagglutinin and neuraminidase, which mediate attachment, entry, and escape. In contrast to influenza A and B, ICV hemagglutinin-esterase-fusion (HEF) glycoprotein, encoded on segment 4, efficiently fulfills the roles of both hemagglutinin and neuraminidase by facilitating host receptor binding, cleaving sialic acid, and membrane fusion[9]. Population immunity may contribute to the variability of ICV[10]. Substantial antigenic and genetic diversity exists among ICV isolates; there are six genetic lineages (C/Taylor, C/Mississippi, C/Aichi, C/Yamagata, C/Kanagawa, and C/Sao Paulo) representing six antigenic groups of HEF, with two major genetic lineages of the internal genes[11-13].
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