Rescue of a Viral Gene from VERO Cells Latently Infected with Influenza Virus B/Lee/40

Tobita, Kiyotake; Tanaka, Toshinori; Hayase, Yukiharu

doi:10.1006/viro.1997.8716

Cited by 11 publications

(10 citation statements)

References 29 publications

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“…Given the lack of error correction for RNA to RNA polymerase, a mutation that dramatically reduces replication errors does not appear plausible. Another possibility is that these viruses have a much lower rate of replication, perhaps because they persist without replicating within host cells or even in the outside environment, but there is no known latency mechanism for RNA viruses, and the very long times (often decades) elapsed between isolations of nearly identical viruses make this kind of mechanism seem somewhat unlikely (12,13,15,(17)(18)(19)(20)(21)24). A recent article argues against the likelihood of influenza virus persistence in the outside environment, such as environmental ice (22).…”

Section: ϫ18mentioning

confidence: 99%

Anomalies in the Influenza Virus Genome Database: New Biology or Laboratory Errors?

Krasnitz

Levine

Rabadán

2008

J Virol

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A search of the influenza virus genome database reveals anomalies associated with a nonnegligible number of submitted sequences. There are many pairs of viral segments that are very close to each other in nucleotide sequence but relatively far apart in reported time of isolation, resulting in an abnormally low evolutionary rate. Also, some sequences show clear evidence of apparent homologous recombination, a process normally assumed to be extremely rare or nonexistent in this virus. These findings may point to surprising new biology but are perhaps more readily explained by stock contamination or other errors in the sequencing laboratories.In the last few years, an extraordinary amount of influenza virus genomic sequence has been submitted to publicly available databases (see, e.g., http://www.ncbi.nlm.nih.gov/genomes /FLU/FLU.html, http://www.flu.lanl.gov, and http://influenza .genomics.org.cn). For instance, there are now over 3,300 full genome sets in the NCBI's rapidly growing Influenza Virus Resource. To our knowledge, no systematic attempt has been made to assess the quality of sequence data in this and similar collections. Our observations show that a fraction of the sequences in the database exhibit anomalous properties that point to either radically new biology or, more likely, problems with the data. As a first example, we consider the rate of nucleotide substitution in the influenza A virus. This rate has been previously estimated at 0.001 to 0.007 per nucleotide per year. (There have been many studies analyzing influenza virus evolutionary rates in different segments and different hosts; see, among others, references 6, 8, 9, 10, 11, 14, and 16.) Using the most conservative (lowest) estimate, we still find many pairs of virus segments that are far closer to each other in nucleotide space than would randomly occur in a Poisson process with this evolutionary rate, given the difference in time of isolation. Such sequences appear to be effectively "frozen in time." For instance, the PB2 segments of isolates A/duck/Taiwan/0526/1972(H6N1) and A/chicken/Taiwan/G23/87(H6N1) differ in only 1 nucleotide position out of 2,283 aligned nucleotides, whereas the expected number of differences, at 0.0015 substitution per nucleotide per year, would be ϳ48 for 15 years. For a null Poisson process, this gives an extremely low P value of 6.6 ϫ 10 Ϫ20

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Section: ϫ18mentioning

confidence: 99%

Anomalies in the Influenza Virus Genome Database: New Biology or Laboratory Errors?

Krasnitz

Levine

Rabadán

2008

J Virol

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“…It has been reported that serum components regulate virus genome expression in acutely and persistently infected cells [23,35,36,39]. Herein, an attempt which was made to clarify the underlying mechanisms of antiviral action of FCS is detailed.…”

Section: Introductionmentioning

confidence: 98%

Fetal calf serum inhibits virus genome expression in Madin-Darby canine kidney cells persistently infected with influenza A virus

Hossain

Mori

Dong

et al. 2007

Med Microbiol Immunol

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A cell line of Madin-Darby canine kidney (MDCK) cells persistently infected with human influenza A virus has been established and designated as MDCK-IVpi cells. Production of progeny virus in MDCK-IVpi cells was suppressed when the cells were incubated in the presence of 10% fetal calf serum (FCS). FCS impaired virus mRNA synthesis in MDCK-IVpi cells, which resulted in a scarcity of virus proteins for virion formation. However, MDCK-IVpi cells well supported the growth of superinfecting heterologous influenza viruses, even in the presence of FCS. A certain fetuin-like substance in FCS might be responsible for the observed inhibition of virus replication.

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“…The protocol and primers (11-84) reported elsewhere [8] were used for reverse transcription followed by nested PCR to detect genes of influenza virus B/Lee/40.…”

Section: Rt-pcrmentioning

confidence: 99%

“…The latter two are have a positive-sense RNA genome [1,2]. Infections with type A and type B influenza viruses are usually acute and lytic, while persistent nonlytic infection can occur in cultured cells [3][4][5][6][7][8] and probably in vivo [9][10][11][12]. In the cells acutely infected with influenza viruses, programmed cell death (apoptosis) is induced [13].…”

Section: Introductionmentioning

confidence: 99%

Characterization of HeLa Cells Persistently Infected with Influenza Virus B/Lee/40 with Respect to Telomerase Activity and Apoptosis

Hayase

Tobita²

2003

Intervirology

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Objective: The purpose of this study was to examine telomerase activity and apoptotic changes in HeLa cells persistently infected with influenza viruses B/Lee/40 (He/Le cells). Methods: He/Le cells were established as described previously [Intervirology 2002;45:67–70], and passaged twice a week. The existence of influenza virus genes was monitored by the reverse transcription polymerase chain reaction (RT-PCR). Telomerase activities in He/Le cells were assayed by Telochaser (stretch PCR method). Apoptotic changes in He/Le cells were examined using the Apoptotic DNA Ladder Kit and the In situ Cell Death Detection Kit, Fluorescence. Results: In He/Le cells, (1) all eight influenza virus genes were detected by RT-PCR until 62 days post infection (p.i.); (2) only nucleoprotein gene remained detectable until 120 days p.i.; (3) telomerase activity of He/Le cells normalized to those of uninfected HeLa cells was remarkably decreased (16–55% of control) during the persistence of influenza and recovered up to 80% of control on day 168 p.i. when no influenza virus gene was detected by RT-PCR, and (4) no apoptotic changes were detected despite the continuous existence of influenza virus genes. Conclusion: In He/Le cells, telomerase activity was suppressed exclusively during the persistence of influenza, and no apoptotic changes were detected.

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Rescue of a Viral Gene from VERO Cells Latently Infected with Influenza Virus B/Lee/40

Cited by 11 publications

References 29 publications

Anomalies in the Influenza Virus Genome Database: New Biology or Laboratory Errors?

Anomalies in the Influenza Virus Genome Database: New Biology or Laboratory Errors?

Fetal calf serum inhibits virus genome expression in Madin-Darby canine kidney cells persistently infected with influenza A virus

Characterization of HeLa Cells Persistently Infected with Influenza Virus B/Lee/40 with Respect to Telomerase Activity and Apoptosis

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