scholarly journals Lianhua-Qingwen Displays Antiviral and Anti-Inflammatory Activity and Synergistic Effects with Oseltamivir against Influenza B Virus Infection in the Mouse Model

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Chunguang Yang ◽  
Yutao Wang ◽  
Jiayang He ◽  
Wen Yan ◽  
Haiming Jiang ◽  
...  

Influenza B virus (IBV) is one of the main pathogens of the annual influenza epidemic, and the disease burden is significant, especially among children and young teenagers. In this study, the antiviral and anti-inflammatory effects of a traditional Chinese medicine prescription, the Lianhua-Qingwen capsule, were evaluated. Our results showed that Lianhua-Qingwen capsule can inhibit both Victoria and Yamagata lineages, and the 50% inhibitive concentrations ranged from 0.228 ± 0.150 to 0.754 ± 0.161 mg/mL. The time course results demonstrated that IBV yields were reduced with treatment at 0–4 h after infection, and the mechanistic research verified that Lianhua-Qingwen capsule has hemagglutination inhibition activity against B/Guangzhou/0215/2012 but not A/California/04/2009. In addition to antiviral activity, Lianhua-Qingwen capsule can also inhibit excessive expression of RANTES, IL-6, IL-8, IP-10, TNF-α, MCP-1, MIP-1β, and IFN-λ at the mRNA level and prevent a severe inflammatory response. The in vivo results confirmed that orally administered Lianhua-Qingwen capsule (100–400 mg/kg/day) does not reduce IBV-induced lung viral load and mortality in mice. However, the pathological change in lungs was alleviated, and there were fewer inflammatory cells in the lungs of Lianhua-Qingwen capsule treated mice than those in controls. Further research confirmed that the combination treatment of 200 mg/kg/day of Lianhua-Qingwen capsule with 2 mg/kg/day of oseltamivir significantly reduced IBV infection over the individual administration of either alone in vivo. Our findings prove that Lianhua-Qingwen capsule could be used as an assistant medicine to enhance the effect of oseltamivir against influenza B virus infection.

2012 ◽  
Vol 205 (6) ◽  
pp. 895-905 ◽  
Author(s):  
Christopher D. Paddock ◽  
Lindy Liu ◽  
Amy M. Denison ◽  
Jeanine H. Bartlett ◽  
Robert C. Holman ◽  
...  

Author(s):  
Pınar YAZICI ÖZKAYA ◽  
Eşe Eda TURANLI ◽  
Hamdi METİN ◽  
Ayça Aydın UYSAL ◽  
Candan ÇİÇEK ◽  
...  

2019 ◽  
Vol 58 (3) ◽  
pp. 441-445 ◽  
Author(s):  
Toshimasa Shimizu ◽  
Naoki Iwamoto ◽  
Momoko Okamoto ◽  
Yushiro Endo ◽  
Sosuke Tsuji ◽  
...  

Vaccine ◽  
2001 ◽  
Vol 19 (11-12) ◽  
pp. 1446-1455 ◽  
Author(s):  
Ze Chen ◽  
Shin-etsu Kadowaki ◽  
Yukari Hagiwara ◽  
Tomoki Yoshikawa ◽  
Tetsutaro Sata ◽  
...  

mBio ◽  
2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Mira C. Patel ◽  
Kari Ann Shirey ◽  
Marina S. Boukhvalova ◽  
Stefanie N. Vogel ◽  
Jorge C. G. Blanco

ABSTRACT Host-derived “danger-associated molecular patterns” (DAMPs) contribute to innate immune responses and serve as markers of disease progression and severity for inflammatory and infectious diseases. There is accumulating evidence that generation of DAMPs such as oxidized phospholipids and high-mobility-group box 1 (HMGB1) during influenza virus infection leads to acute lung injury (ALI). Treatment of influenza virus-infected mice and cotton rats with the Toll-like receptor 4 (TLR4) antagonist Eritoran blocked DAMP accumulation and ameliorated influenza virus-induced ALI. However, changes in systemic HMGB1 kinetics during the course of influenza virus infection in animal models and humans have yet to establish an association of HMGB1 release with influenza virus infection. To this end, we used the cotton rat model that is permissive to nonadapted strains of influenza A and B viruses, respiratory syncytial virus (RSV), and human rhinoviruses (HRVs). Serum HMGB1 levels were measured by an enzyme-linked immunosorbent assay (ELISA) prior to infection until day 14 or 18 post-infection. Infection with either influenza A or B virus resulted in a robust increase in serum HMGB1 levels that decreased by days 14 to 18. Inoculation with the live attenuated vaccine FluMist resulted in HMGB1 levels that were significantly lower than those with infection with live influenza viruses. RSV and HRVs showed profiles of serum HMGB1 induction that were consistent with their replication and degree of lung pathology in cotton rats. We further showed that therapeutic treatment with Eritoran of cotton rats infected with influenza B virus significantly blunted serum HMGB1 levels and improved lung pathology, without inhibiting virus replication. These findings support the use of drugs that block HMGB1 to combat influenza virus-induced ALI. IMPORTANCE Influenza virus is a common infectious agent causing serious seasonal epidemics, and there is urgent need to develop an alternative treatment modality for influenza virus infection. Recently, host-derived DAMPs, such as oxidized phospholipids and HMGB1, were shown to be generated during influenza virus infection and cause ALI. To establish a clear link between influenza virus infection and HMGB1 as a biomarker, we have systematically analyzed temporal patterns of serum HMGB1 release in cotton rats infected with nonadapted strains of influenza A and B viruses and compared these patterns with a live attenuated influenza vaccine and infection by other respiratory viruses. Towards development of a new therapeutic modality, we show herein that blocking serum HMGB1 levels by Eritoran improves lung pathology in influenza B virus-infected cotton rats. Our study is the first report of systemic HMGB1 as a potential biomarker of severity in respiratory virus infections and confirms that drugs that block virus-induced HMGB1 ameliorate ALI.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (2) ◽  
pp. 225-229
Author(s):  
Teri Jo Mauch ◽  
Tim Myers ◽  
Clifford E. Kashtan ◽  
Susan Bratton ◽  
Elliot Krane ◽  
...  

Objective. Influenza B virus causes epidemic infection in normal children, but only one case of infection in an immunocompromised solid organ transplant (SOT) recipient has been reported. Characterization of the clinical course of influenza B virus infection in pediatric SOT recipients may increase the utilization of preventive and therapeutic interventions by pediatricians caring for these immunocompromised children. Design. Retrospective chart review of patients whose respiratory viral cultures yielded influenza B from January 1989 through March 1992. Patients. Twelve pediatric SOT recipients with influenza B virus infection were identified. These included five renal, four hepatic, and three cardiac allograft recipients, ranging from 19 months to 17 years 9 months of age (median 6 years 2 months). The post-transplant interval ranged from 6 weeks to 4 years 6 months (average 26.7 months). No patient had been immunized against influenza. Exposure histories were documented for eight children; five of these occurred in the hospital. Results. Clinical symptoms included fever (12/12), respiratory (11/12), or gastrointestinal complaints (8/12). Five patients had neurologic involvement; one died of uncal herniation. Ten children were hospitalized (median duration, 3 days; range, 2 to 79 days). Two patients (post-transplant interval, 3 to 8 months) required mechanical ventilation, and one of these received aerosolized ribavirin. Three children had concurrent allograft rejection. Conclusions. Influenza B infection is potentially life-threatening in pediatric SOT recipients. We recommend annual immunization of pediatric SOT recipients, their household contacts, and health care workers. Prospective studies are needed to evaluate the efficacy of influenza vaccination in pediatric SOT recipients.


2008 ◽  
Vol 82 (21) ◽  
pp. 10580-10590 ◽  
Author(s):  
Rong Hai ◽  
Luis Martínez-Sobrido ◽  
Kathryn A. Fraser ◽  
Juan Ayllon ◽  
Adolfo García-Sastre ◽  
...  

ABSTRACT Type B influenza viruses can cause substantial morbidity and mortality in the population, and vaccination remains by far the best means of protection against infections with these viruses. Here, we report the construction of mutant influenza B viruses for potential use as improved live-virus vaccine candidates. Employing reverse genetics, we altered the NS1 gene, which encodes a type I interferon (IFN) antagonist. The resulting NS1 mutant viruses induced IFN and, as a consequence, were found to be attenuated in vitro and in vivo. The absence of pathogenicity of the NS1 mutants in both BALB/c and C57BL/6 PKR−/− mice was confirmed. We also provide evidence that influenza B virus NS1 mutants induce a self-adjuvanted immune response and confer effective protection against challenge with both homologous and heterologous B virus strains in mice.


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