scholarly journals Pulmonary Collectins Modulate Strain-Specific Influenza A Virus Infection and Host Responses

2004 ◽  
Vol 78 (16) ◽  
pp. 8565-8572 ◽  
Author(s):  
Samuel Hawgood ◽  
Cynthia Brown ◽  
Jess Edmondson ◽  
Amber Stumbaugh ◽  
Lennell Allen ◽  
...  

ABSTRACT Collectins are secreted collagen-like lectins that bind, agglutinate, and neutralize influenza A virus (IAV) in vitro. Surfactant proteins A and D (SP-A and SP-D) are collectins expressed in the airway and alveolar epithelium and could have a role in the regulation of IAV infection in vivo. Previous studies have shown that binding of SP-D to IAV is dependent on the glycosylation of specific sites on the HA1 domain of hemagglutinin on the surface of IAV, while the binding of SP-A to the HA1 domain is dependent on the glycosylation of the carbohydrate recognition domain of SP-A. Here, using SP-A and SP-D gene-targeted mice on a common C57BL6 background, we report that viral replication and the host response as measured by weight loss, neutrophil influx into the lung, and local cytokine release are regulated by SP-D but not SP-A when the IAV is glycosylated at a specific site (N165) on the HA1 domain. SP-D does not protect against IAV infection with a strain lacking glycosylation at N165. With the exception of a small difference on day 2 after infection with X-79, we did not find any significant difference in viral load in SP-A−/− mice with either IAV strain, although small differences in the cytokine responses to IAV were detected in SP-A−/− mice. Mice deficient in both SP-A and SP-D responded to IAV similarly to mice deficient in SP-D alone. Since most strains of IAV currently circulating are glycosylated at N165, SP-D may play a role in protection from IAV infection.

2014 ◽  
Vol 5 ◽  
Author(s):  
Emanuel Haasbach ◽  
Carmen Hartmayer ◽  
Alice Hettler ◽  
Alicja Sarnecka ◽  
Ulrich Wulle ◽  
...  

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1630 ◽  
Author(s):  
Junu A. George ◽  
Shaikha H. AlShamsi ◽  
Maryam H. Alhammadi ◽  
Ahmed R. Alsuwaidi

Influenza A virus (IAV) and respiratory syncytial virus (RSV) are leading causes of childhood infections. RSV and influenza are competitive in vitro. In this study, the in vivo effects of RSV and IAV co-infection were investigated. Mice were intranasally inoculated with RSV, with IAV, or with both viruses (RSV+IAV and IAV+RSV) administered sequentially, 24 h apart. On days 3 and 7 post-infection, lung tissues were processed for viral loads and immune cell populations. Lung functions were also evaluated. Mortality was observed only in the IAV+RSV group (50% of mice did not survive beyond 7 days). On day 3, the viral loads in single-infected and co-infected mice were not significantly different. However, on day 7, the IAV titer was much higher in the IAV+RSV group, and the RSV viral load was reduced. CD4 T cells were reduced in all groups on day 7 except in single-infected mice. CD8 T cells were higher in all experimental groups except the RSV-alone group. Increased airway resistance and reduced thoracic compliance were demonstrated in both co-infected groups. This model indicates that, among all the infection types we studied, infection with IAV followed by RSV is associated with the highest IAV viral loads and the most morbidity and mortality.


2014 ◽  
Vol 455 (1) ◽  
pp. 80-83 ◽  
Author(s):  
P. G. Deryabin ◽  
G. A. Galegov ◽  
I. D. Konstantinova ◽  
I. S. Muzyka ◽  
A. I. Miroshnikov ◽  
...  

2016 ◽  
Vol 185 ◽  
pp. 327-340 ◽  
Author(s):  
Amin Haghani ◽  
Parvaneh Mehrbod ◽  
Nikoo Safi ◽  
Nur Ain Aminuddin ◽  
Azadeh Bahadoran ◽  
...  

2020 ◽  
Author(s):  
Mengwei Li ◽  
Yuxu Wang ◽  
Jing Jin ◽  
Jie Dou ◽  
Qinglong Guo ◽  
...  

Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1171
Author(s):  
Yaron Drori ◽  
Jasmine Jacob-Hirsch ◽  
Rakefet Pando ◽  
Aharona Glatman-Freedman ◽  
Nehemya Friedman ◽  
...  

Influenza viruses and respiratory syncytial virus (RSV) are respiratory viruses that primarily circulate worldwide during the autumn and winter seasons. Seasonal surveillance has shown that RSV infection generally precedes influenza. However, in the last four winter seasons (2016–2020) an overlap of the morbidity peaks of both viruses was observed in Israel, and was paralleled by significantly lower RSV infection rates. To investigate whether the influenza A virus inhibits RSV, human cervical carcinoma (HEp2) cells or mice were co-infected with influenza A and RSV. Influenza A inhibited RSV growth, both in vitro and in vivo. Mass spectrometry analysis of mouse lungs infected with influenza A identified a two-wave pattern of protein expression upregulation, which included members of the interferon-induced protein with the tetratricopeptide (IFITs) family. Interestingly, in the second wave, influenza A viruses were no longer detectable in mouse lungs. In addition, knockdown and overexpression of IFITs in HEp2 cells affected RSV multiplicity. In conclusion, influenza A infection inhibits RSV infectivity via upregulation of IFIT proteins in a two-wave modality. Understanding the immune system involvement in the interaction between influenza A and RSV viruses will contribute to the development of future treatment strategies against these viruses.


2019 ◽  
Vol 61 (3) ◽  
pp. 395-398
Author(s):  
Christin Peteranderl ◽  
Irina Kuznetsova ◽  
Jessica Schulze ◽  
Martin Hardt ◽  
Emilia Lecuona ◽  
...  

2001 ◽  
Vol 52 (1) ◽  
pp. 43-53 ◽  
Author(s):  
A Horváth ◽  
I Andersen ◽  
K Junker ◽  
B Lyck Fogh-Schultz ◽  
E Holm Nielsen ◽  
...  

2000 ◽  
Vol 44 (1) ◽  
pp. 200-204 ◽  
Author(s):  
Francesca Pica ◽  
Anna Teresa Palamara ◽  
Antonio Rossi ◽  
Alessandra De Marco ◽  
Carla Amici ◽  
...  

ABSTRACT 9-Deoxy-Δ9,Δ12-13,14-dihydro-prostaglandin D2 (Δ12-PGJ2), a natural cyclopentenone metabolite of prostaglandin D2, is shown to possess therapeutic efficacy against influenza A virus A/PR8/34 (H1N1) infection in vitro and in vivo. The results indicate that the antiviral activity is associated with induction of cytoprotective heat shock proteins and suggest novel strategies for treatment of influenza virus infection.


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