A Nationwide Epidemic of Influenza C Virus Infection in Japan in 2004

Matsuzaki, Yoko; Abiko, Chieko; Mizuta, Katsumi; Sugawara, Kanetsu; Takashita, Emi; Muraki, Yasushi; Sano, Hiroshi; Mikawa, Masahide; Shimada, Shin‐ichi; Sato, Katsuhiko; Kuzuya, Mitsutaka; Takao, Shinichi; Wakatsuki, Kiyoko; Itagaki, Tsutomu; Hongō, Seiji; Nishimura, Hidekazu

doi:10.1128/jcm.01555-06

Cited by 55 publications

(73 citation statements)

References 21 publications

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“…In this same time period, the dominant FLUCV strain circulating in Japan belonged to the C/Brazil‐Sao Paulo/378/82‐related lineage,6 while in Caen, France, two dominant strains of the C/Brazil‐Sao Paulo/378/82 and C/Japan‐Yamagata/26/81‐related lineages were found to be cocirculating 4. This suggests that the worldwide distribution of FLUCV may vary, with each geographical location presenting a different predominant strain in the same timeframe.…”

Section: Discussionmentioning

confidence: 90%

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Genetic characterisation of influenza C viruses detected in Singapore in 2006

Ting

Seah

Lim

et al. 2015

Influenza Resp Viruses

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In an earlier study on respiratory infections in Singapore military recruits, four influenza C virus (FLUCV) infections were detected out of the 1354 samples collected. All four isolates were detected in 2006, and their whole genome was completely sequenced and analysed. Phylogenetic analysis of the hemagglutinin esterase fusion (HEF) gene revealed that all four Singapore isolates belonged to the C/Japan‐Kanagawa/1/76‐related lineage. However, the genes of the four FLUCV isolates had origins from several different lineages, and the genome composition resembles that of the C/Japan‐Miyagi/9/96‐like strains that had been circulating in Japan between 1996 and 2000.

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Section: Discussionmentioning

confidence: 90%

“…Although influenza A, B and C viruses belong to the same Orthomyxoviridae family, current epidemiological research tend to focus more on FLUAV and FLUBV. Outbreaks of influenza C virus (FLUCV) infections have been detected mainly in Japan and reported elsewhere for example in France 4, 5, 6…”

Section: Introductionmentioning

confidence: 99%

Genetic characterisation of influenza C viruses detected in Singapore in 2006

Ting

Seah

Lim

et al. 2015

Influenza Resp Viruses

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“…To determine whether hemagglutinin-esterase-fusion protein (HEF), a surface glycoprotein of influenza C virus, is a restricting factor for this temperature sensitivity, we analyzed the biological and biochemical properties of HEF at 33°C and 37°C. We found that HEF exhibits intrinsic temperature sensitivities for surface expression and fusion activity.T he optimum temperature for the replication of influenza C viruses, which cause mainly upper respiratory tract diseases (7,8), is around 32 to 33°C (12,19). Studies have demonstrated that influenza C viral RNA polymerase has higher activity at 33°C than at 37°C (10,11).…”

mentioning

confidence: 99%

“…T he optimum temperature for the replication of influenza C viruses, which cause mainly upper respiratory tract diseases (7,8), is around 32 to 33°C (12,19). Studies have demonstrated that influenza C viral RNA polymerase has higher activity at 33°C than at 37°C (10,11).…”

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confidence: 99%

Intrinsic Temperature Sensitivity of Influenza C Virus Hemagglutinin-Esterase-Fusion Protein

Takashita

Muraki

Sugawara

et al. 2012

J Virol

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m Influenza C virus replicates more efficiently at 33°C than at 37°C. To determine whether hemagglutinin-esterase-fusion protein (HEF), a surface glycoprotein of influenza C virus, is a restricting factor for this temperature sensitivity, we analyzed the biological and biochemical properties of HEF at 33°C and 37°C. We found that HEF exhibits intrinsic temperature sensitivities for surface expression and fusion activity.T he optimum temperature for the replication of influenza C viruses, which cause mainly upper respiratory tract diseases (7,8), is around 32 to 33°C (12,19). Studies have demonstrated that influenza C viral RNA polymerase has higher activity at 33°C than at 37°C (10,11). To obtain further insights into the intrinsic temperature sensitivities of influenza C viruses, we investigated hemagglutinin-esterase-fusion protein (HEF), an influenza C virus glycoprotein (14). HEF is the counterpart of both hemagglutinin (HA) and neuraminidase (NA) in influenza A and B viruses and has three biological properties: receptor binding, receptor destruction, and membrane fusion activity (5, 13).To examine whether influenza C virus grows better at a lower temperature due to its HEF functions, African green monkey kidney-derived CV-1 cells were infected with C/Ann Arbor/1/50 (C/AA50) virus at a multiplicity of infection (MOI) of 10 and cultured at either 33°C or 37°C. At 48 h postinfection, infected cells were treated with tosylsulfonyl phenylalanyl chloromethyl ketone (TPCK)-trypsin and exposed to fusion buffer (phosphate-buffered saline with 10 mM morpholineethanesulfonic acid and 10 mM HEPES; adjusted to pH 5.0). After a 4-h incubation, polykaryon formation was examined under a microscope. We found that polykaryons were formed in 75% of the cells at 33°C compared with 35% of the cells at 37°C (Fig. 1A). We then analyzed HEF expression levels on infected cells by flow cytometry with the anti-HEF monoclonal antibody (MAb) clone J14 (17). The HEF cell surface expression level at 33°C was twice that at 37°C (Fig. 1B). These results suggest that the better growth of influenza C virus at the lower temperature is associated with HEF functions.To determine whether intrinsic HEF biologic properties contribute to the temperature sensitivity of this virus, we wanted to rule out the influence of other viral proteins on HEF expression and/or function. To this end, we expressed C/AA50 HEF by using a protein expression plasmid, pME18S/HEF-AA (9). HEF expression from this plasmid was controlled by an RNA polymerase II-driven simian virus 40 early promoter. To test the effect of temperature on HEF expression, COS-1 cells, derivatives of CV-1 cells with a high transfection efficiency, were transfected with the plasmid and cultured at 37°C for 24 h, followed by either further incubation at 37°C or a temperature shift to 33°C. At 24 and 48 h posttransfection (hpt), transfected cells were labeled with [35 S]methionine for 20 min. Cell lysates were immunoprecipitated with anti-HEF MAb D37 (18) and analyzed by means of sodium dodecyl su...

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“…Wirusy te wywołują łagodne infekcje górnych dróg oddechowych, zwłaszcza u dzieci, a przeciwciała dla tego typu są wykrywane u większości osób starszych oraz u dzieci. Były one także izolowane w czasie epidemii grypy wywołanych przez IAV oraz IBV (1,15). Szczepy ICV izolowane od ludzi reprezentują jeden podtyp, wykazują niski poziom zmienności genetycznej i ewoluują około dziewięciokrotnie wolniej niż IAV.…”

Section: Wirusy Grypy Typu Bunclassified

Characterization of a new influenza virus type D

Markowska-Daniel¹,

Mickiewicz²,

Witkowski³

et al. 2016

Medycyna Weterynaryjna

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Influenza is caused by viruses belonging to the Orthomyxoviridae family. Currently three types of influenza virus are known: A (Influenza A virus, IAV), B (IBV) and C (ICV). Despite the fact that all these viruses are derived from a common ancestor they differ from each other by the number of segments, the size and sequence of RNA segments, antigenicity, pathogenicity and the spectrum of natural reservoirs. In 2011, a new influenza virus was isolated in the USA from pigs manifesting influenza-like symptoms. The virus was the most closely related to ICV. It was able to replicate in vitro in different cell cultures and displayed much broader cell tropism than human ICV. Moreover, in contrast to ICV, it was able to replicate at 370C. Electron microscopic studies demonstrated features characteristic of Orthomyxoviruses. Despite morphological and organizational similarities, the biological properties of the new virus, including biochemical activity, differ from that of other influenza viruses. Enzymatic assays revealed that the new virus had negligible neuraminidase but detectable O-acetyloesterase activity. Further studies evidenced that the new virus varied from ICV in receptor binding, despite its sharing a conserved array of functional domains in the viral RNA genome replication and viral entry machinery. Analysis conducted with the use of the model of crystal structure of the hemagglutinin-esterase fusion protein (HE) of the new virus and its receptor demonstrated that this protein was multifunctional. It catalyzes cellular receptor binding, receptor cleavage, as well as membrane fusion. Moreover, divergent receptor-binding sites than HE of ICV have been discovered in the new virus. These amino acid differences may alter the binding specificity and affinity of the HE protein to the receptor that in turn result in the observed differences in cellular tropism between the two viruses. It also possesses an open channel between the 230-helix and 270-loop in the receptor-binding site, which is a unique feature of this virus. This might explain why the new virus has a broad cell tropism. It is possible that the sequence variation in the fusion domain may influence the replication of this virus at a higher temperature when compared to ICV. Next-generation sequencing demonstrated that the genome of the new virus, similarly to ICV, had seven single-stranded negative-sense RNA segments coding 9 viral proteins. Deep RNA sequencing found a M1 protein expression strategy different from that of ICV. Studies aimed at evaluating of the evolutionary relationship of both viruses revealed that the new virus and ICV shared an approximately 69-72% mean pairwise identity in the PB1 gene, which is reported to be the most conserved influenza virus protein. Additionally, differences were detected at 5’ and 3’ends of noncoding regions, which are also highly conserved. They both may be responsible for the lack of in vitro reassortment between ICV of human origin and the new virus. In the study characterizing antigenic properties of the new virus, no cross-reactivity was observed using HI and AGID tests. This indicates the major differences in conserved proteins M1 and NP between both viruses. Summing up, despite the fact that new virus is the most closely related to human ICV, the number of important antigenic and genetic distinctions among them is the basis for suggesting that the International Committee of Virus Taxonomy classify it as a separate genus - D. There is no doubt that the discovery of a new influenza virus genus will have a great impact on influenza research and ecology.

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A Nationwide Epidemic of Influenza C Virus Infection in Japan in 2004

Cited by 55 publications

References 21 publications

Genetic characterisation of influenza C viruses detected in Singapore in 2006

Genetic characterisation of influenza C viruses detected in Singapore in 2006

Intrinsic Temperature Sensitivity of Influenza C Virus Hemagglutinin-Esterase-Fusion Protein

Characterization of a new influenza virus type D

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