Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2

Goto, Hideo; Ihira, Hironobu; Morishita, Keiichi; Tsuchiya, Mitsuki; Ohta, Keisuke; Yumine, Natsuko; Tsurudome, Masato; Nishio, Machiko

doi:10.1007/s00430-015-0441-y

Cited by 41 publications

(64 citation statements)

References 52 publications

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“…Coinfection of single cells was excluded. The model replicated in vitro data from coinfection with IAV and RSV, where IAV inhibits RSV growth, and with IAV and PIV, where PIV enhances IAV growth . A key result was that varied infection kinetics and outcomes could manifest from changing the virus dose or the intrinsic virus growth rate.…”

Section: Viral–viral Coinfection Kineticsmentioning

confidence: 55%

“…Some responses (eg, IFN) may have dynamics that are virus‐specific, and the resulting interactions depend on the pathogen strain, dose, and order. For example, PIVs can increase the rate of IAV growth by fusing cells together and facilitating cell‐to‐cell spread . This occurs without any noticeable effect on PIV replication.…”

Section: Viral–viral Coinfection Kineticsmentioning

confidence: 99%

“…Influenza viruses that cause severe disease support higher incidence of bacterial coinfection, yet only a proportion of infections result in a coinfection . Furthermore, other respiratory viruses may also coinfect and enhance influenza‐related disease . Factors that impact influenza severity and, thus, coinfection risk are not well understood.…”

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

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Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

Smith

2018

Immunological Reviews

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SummaryInfluenza virus infections are a leading cause of morbidity and mortality worldwide. This is due in part to the continual emergence of new viral variants and to synergistic interactions with other viruses and bacteria. There is a lack of understanding about how host responses work to control the infection and how other pathogens capitalize on the altered immune state. The complexity of multi‐pathogen infections makes dissecting contributing mechanisms, which may be non‐linear and occur on different time scales, challenging. Fortunately, mathematical models have been able to uncover infection control mechanisms, establish regulatory feedbacks, connect mechanisms across time scales, and determine the processes that dictate different disease outcomes. These models have tested existing hypotheses and generated new hypotheses, some of which have been subsequently tested and validated in the laboratory. They have been particularly a key in studying influenza‐bacteria coinfections and will be undoubtedly be useful in examining the interplay between influenza virus and other viruses. Here, I review recent advances in modeling influenza‐related infections, the novel biological insight that has been gained through modeling, the importance of model‐driven experimental design, and future directions of the field.

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Section: Viral–viral Coinfection Kineticsmentioning

confidence: 55%

Section: Viral–viral Coinfection Kineticsmentioning

confidence: 99%

Section: Concluding Remarks and Perspectivesmentioning

confidence: 99%

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Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

Smith

2018

Immunological Reviews

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“…However, they found that inoculation of IAV 12 h after RSV significantly lowered IAV titers, suggesting that depletion of target cells, and not direct interference, was responsible (37). In contrast, in vitro coinfection by parainfluenza virus (parainfluenza virus type 2 [PIV2]) has been shown to enhance IAV infection, which is dependent on the cell-cell fusion activity of PIV2 (38). Our previous studies have shown that RV induces a robust type I IFN response in the LA-4 cell line (33); thus, the lack of PR8 inhibition in vitro is likely not due to the absence of an IFN response.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Influenza A Virus Disease Severity by Viral Coinfection in a Mouse Model

González

Ijezie

Balemba

et al. 2018

J Virol

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Influenza viruses and rhinoviruses are responsible for a large number of acute respiratory viral infections in human populations and are detected as copathogens within hosts. Clinical and epidemiological studies suggest that coinfection by rhinovirus and influenza virus may reduce disease severity and that they may also interfere with each other's spread within a host population. To determine how coinfection by these two unrelated respiratory viruses affects pathogenesis, we established a mouse model using a minor serogroup rhinovirus (rhinovirus strain 1B [RV1B]) and mouse-adapted influenza A virus (A/Puerto Rico/8/1934 [PR8]). Infection of mice with RV1B 2 days before PR8 reduced the severity of infection by a low or medium, but not high, dose of PR8. Disease attenuation was associated with an early inflammatory response in the lungs and enhanced clearance of PR8. However, coinfection by RV1B did not reduce PR8 viral loads early in infection or inhibit replication of PR8 within respiratory epithelia or Inflammation in coinfected mice remained focal compared to diffuse inflammation and damage in the lungs of mice infected by PR8. The timing of RV1B coinfection was a critical determinant of protection, suggesting that sufficient time is needed to induce this response. Finally, disease attenuation was not unique to RV1B: dose-dependent coinfection by a murine coronavirus (mouse hepatitis virus strain 1 [MHV-1]) also reduced the severity of PR8 infection. Unlike RV1B, coinfection with MHV-1 reduced early PR8 replication, which was associated with upregulation of beta interferon (IFN-β) expression. This model is critical for understanding the mechanisms responsible for influenza disease attenuation during coinfection by unrelated respiratory viruses. Viral infections in the respiratory tract can cause severe disease and are responsible for a majority of pediatric hospitalizations. Molecular diagnostics have revealed that approximately 20% of these patients are infected by more than one unrelated viral pathogen. To understand how viral coinfection affects disease severity, we inoculated mice with a mild viral pathogen (rhinovirus or murine coronavirus), followed 2 days later by a virulent viral pathogen (influenza A virus). This model demonstrated that rhinovirus can reduce the severity of influenza A virus, which corresponded with an early but controlled inflammatory response in the lungs and early clearance of influenza A virus. We further determined the dose and timing parameters that were important for effective disease attenuation and showed that influenza disease is also reduced by coinfection with a murine coronavirus. These findings demonstrate that coinfecting viruses can alter immune responses and pathogenesis in the respiratory tract.

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“…Likewise, La Crosse virus (LACV) and Sindbis virus (SINV) coinfection in C6/36 cells resulted in enhanced SINV replication (166). In a study by Goto et al, human parainfluenza virus 2 (hPIV2) infection-associated cell fusion facilitated IAV replication and modulated pathological consequences (197). In another study, the simultaneous inoculation of culex flavivirus (CxFV) and West Nile virus (WNV) facilitated WNV transmission (168), although prior infection with CxFV had no effect on WNV replication.…”

Section: Enhanced Virus Replicationmentioning

confidence: 99%

Virological and Immunological Outcomes of Coinfections

et al. 2018

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SUMMARYCoinfections involving viruses are being recognized to influence the disease pattern that occurs relative to that with single infection. Classically, we usually think of a clinical syndrome as the consequence of infection by a single virus that is isolated from clinical specimens. However, this biased laboratory approach omits detection of additional agents that could be contributing to the clinical outcome, including novel agents not usually considered pathogens. The presence of an additional agent may also interfere with the targeted isolation of a known virus. Viral interference, a phenomenon where one virus competitively suppresses replication of other coinfecting viruses, is the most common outcome of viral coinfections. In addition, coinfections can modulate virus virulence and cell death, thereby altering disease severity and epidemiology. Immunity to primary virus infection can also modulate immune responses to subsequent secondary infections. In this review, various virological mechanisms that determine viral persistence/exclusion during coinfections are discussed, and insights into the isolation/detection of multiple viruses are provided. We also discuss features of heterologous infections that impact the pattern of immune responsiveness that develops.

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Enhanced growth of influenza A virus by coinfection with human parainfluenza virus type 2

Cited by 41 publications

References 52 publications

Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

Host‐pathogen kinetics during influenza infection and coinfection: insights from predictive modeling

Attenuation of Influenza A Virus Disease Severity by Viral Coinfection in a Mouse Model

Virological and Immunological Outcomes of Coinfections

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