scholarly journals Active Components of Commonly Prescribed Medicines Affect Influenza A Virus–Host Cell Interaction: A Pilot Study

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1537
Author(s):  
Aleksandr Ianevski ◽  
Rouan Yao ◽  
Eva Zusinaite ◽  
Hilde Lysvand ◽  
Valentyn Oksenych ◽  
...  
Keyword(s):  
Host Cell ◽  
Influenza A Virus ◽  
Drug Target ◽  
Influenza A ◽  
Cell Interaction ◽  
Host Responses ◽  
Target Interaction ◽  
Prescribed Medicines ◽  
Host Cell Interaction

Background: Every year, millions of people are hospitalized and thousands die from influenza A virus (FLUAV) infection. Most cases of hospitalizations and death occur among the elderly. Many of these elderly patients are reliant on medical treatment of underlying chronic diseases, such as arthritis, diabetes, and hypertension. We hypothesized that the commonly prescribed medicines for treatment of underlying chronic diseases can affect host responses to FLUAV infection and thus contribute to the morbidity and mortality associated with influenza. Therefore, the aim of this study was to examine whether commonly prescribed medicines could affect host responses to virus infection in vitro. Methods: We first identified 45 active compounds from a list of commonly prescribed medicines. Then, we constructed a drug–target interaction network and identified the potential implication of these interactions for FLUAV–host cell interplay. Finally, we tested the effect of 45 drugs on the viability, transcription, and metabolism of mock- and FLUAV-infected human retinal pigment epithelial (RPE) cells. Results: In silico drug–target interaction analysis revealed that drugs such as atorvastatin, candesartan, and hydroxocobalamin could target and modulate FLUAV–host cell interaction. In vitro experiments showed that at non-cytotoxic concentrations, these compounds affected the transcription and metabolism of FLUAV- and mock-infected cells. Conclusion: Many commonly prescribed drugs were found to modulate FLUAV–host cell interactions in silico and in vitro and could therefore affect their interplay in vivo, thus contributing to the morbidity and mortality of patients with influenza virus infections.

scholarly journals Active Components of Commonly Prescribed Medicines Affect Influenza a Virus-Host Cell Interaction: A Pilot Study

2021 ◽  
Author(s):  
Aleksandr Ianevski ◽  
Rouan Yao ◽  
Eva Zusinaite ◽  
Hilde Lysvand ◽  
Valentyn Oksenych ◽  
...  
Keyword(s):  
Host Cell ◽  
Influenza A Virus ◽  
Drug Target ◽  
Influenza A ◽  
Cell Interaction ◽  
Host Responses ◽  
Target Interaction ◽  
Prescribed Medicines ◽  
Host Cell Interaction

Background: Every year, millions of people are hospitalized, and thousands die from influenza A virus (FLUAV) infection. Most cases of hospitalizations and death occur among elderly. Many of these elderly patients are reliant on medical treatment of underlying chronic diseases, such as arthritis, diabetes, and hypertension. We hypothesized that the commonly prescribed medicines for treatment of underlying chronic diseases can affect host responses to FLUAV infection, and thus contribute to morbidity and mortality associated with influenza. Therefore, the aim of this study was to examine whether commonly prescribed medicines could affect host responses to virus infection in vitro. Methods: We first identified 45 active compounds of medicines commonly prescribed in Central Norway. Then we constructed a drug-target interaction network and identified potential implication of these interactions for FLUAV-host cell interplay. Finally, we tested the effect of 45 drugs on viability, transcription and metabolism of mock- and A/WSN/33(H1N1)-infected human retinal pigment epithelial (RPE) cells. Results: In silico drug-target interaction analysis revealed that many drugs, such as acetylsalicylic acid, atorvastatin, candesartan, and hydroxocobalam, could target and modulate FLUAV-host cell interaction. In vitro experiments showed that these and other compounds at non-cytotoxic concentrations differently affected transcription and metabolism of mock- and FLUAV-infected cells. Conclusion: Many commonly prescribed drugs modulate FLUAV-host cell interactions in vitro and therefore could affect their interplay in vivo, thus, contributing to morbidity and mortality of patients with influenza virus infections.

scholarly journals Active components of commonly prescribed medicines affect influenza A virus-host cell interaction: a pilot study

2021 ◽  
Author(s):  
Aleksandr Ianevski ◽  
Rouan Yao ◽  
Eva Zusinaite ◽  
Hilde Lysvand ◽  
Valentyn Oksenych ◽  
...  
Keyword(s):  
Host Cell ◽  
Influenza A Virus ◽  
Drug Target ◽  
Influenza A ◽  
Cell Interaction ◽  
Host Responses ◽  
Target Interaction ◽  
Prescribed Medicines ◽  
Host Cell Interaction

Background: Every year, millions of people are hospitalized, and thousands die from influenza A virus (FLUAV) infection. Most cases of hospitalizations and death occur among elderly. Many of these elderly patients are reliant on medical treatment of underlying chronic diseases, such as arthritis, diabetes, and hypertension. We hypothesized that the commonly prescribed medicines for treatment of underlying chronic diseases can affect host responses to FLUAV infection, and thus contribute to morbidity and mortality associated with influenza. Therefore, the aim of this study was to examine whether commonly prescribed medicines could affect host responses to virus infection in vitro. Methods: We first identified 45 active compounds of commonly prescribed medicines. Then we constructed a drug-target interaction network and identified potential implication of these interactions for FLUAV-host cell interplay. Finally, we tested the effect of 45 drugs on viability, transcription and metabolism of mock- and FLUAV-infected human retinal pigment epithelial (RPE) cells. Results: In silico drug-target interaction analysis revealed that many drugs, such as atorvastatin, candesartan, and hydroxocobalam, could target and modulate FLUAV-host cell interaction. In vitro experiments showed that these and other compounds at non-cytotoxic concentrations differently affected transcription and metabolism of mock- and FLUAV-infected cells. Conclusion: Many commonly prescribed drugs modulate FLUAV-host cell interactions in silico and in vitro and, therefore, could affect their interplay in vivo, thus, contributing to morbidity and mortality of patients with influenza virus infections.

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 ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Host Response ◽  
Influenza A ◽  
Small Difference ◽  
Alveolar Epithelium ◽  
Host Responses ◽  
Cytokine Release ◽  
Significant Difference

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.

scholarly journals Improved enzyme-linked immunoadsorbent assay (ELISA) for the study of Trypanosoma cruzi-host cell interaction in vitro

1993 ◽  
Vol 88 (2) ◽  
pp. 235-241 ◽  
Author(s):  
Mauricio R. M. P. Luz ◽  
Maria de Nazaré C. Soeiro ◽  
Tania C. Araújo-Jorge
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Cell Interaction ◽  
Host Cell Interaction

scholarly journals Advances in Zika Virus–Host Cell Interaction: Current Knowledge and Future Perspectives

2019 ◽  
Vol 20 (5) ◽  
pp. 1101 ◽  
Author(s):  
Jae Lee ◽  
Ok Shin
Keyword(s):  
Host Cell ◽  
Zika Virus ◽  
Current Knowledge ◽  
Cell Interaction ◽  
Human Pathogens ◽  
Zikv Infection ◽  
In Vivo Models ◽  
Host Cell Interaction

Emerging mosquito-transmitted RNA viruses, such as Zika virus (ZIKV) and Chikungunya represent human pathogens of an immense global health problem. In particular, ZIKV has emerged explosively since 2007 to cause a series of epidemics in the South Pacific and most recently in the Americas. Although typical ZIKV infections are asymptomatic, ZIKV infection during pregnancy is increasingly associated with microcephaly and other fetal developmental abnormalities. In the last few years, genomic and molecular investigations have established a remarkable progress on the pathogenic mechanisms of ZIKV infection using in vitro and in vivo models. Here, we highlight recent advances in ZIKV-host cell interaction studies, including cellular targets of ZIKV, ZIKV-mediated cell death mechanisms, host cell restriction factors that limit ZIKV replication, and immune evasion mechanisms utilized by ZIKV. Understanding of the mechanisms of ZIKV–host interaction at the cellular level will contribute crucial insights into the development of ZIKV therapeutics and vaccines.

scholarly journals Akt Inhibitor MK2206 Prevents Influenza pH1N1 Virus InfectionIn Vitro

2014 ◽  
Vol 58 (7) ◽  
pp. 3689-3696 ◽  
Author(s):  
Oxana V. Denisova ◽  
Sandra Söderholm ◽  
Salla Virtanen ◽  
Carina Von Schantz ◽  
Dmitrii Bychkov ◽  
...  
Keyword(s):  
Virus Infection ◽  
Host Cell ◽  
Treatment Options ◽  
Cell Interaction ◽  
Akt Signaling ◽  
Akt Inhibitor ◽  
Prevention And Treatment ◽  
Host Cell Interaction

ABSTRACTThe influenza pH1N1 virus caused a global flu pandemic in 2009 and continues manifestation as a seasonal virus. Better understanding of the virus-host cell interaction could result in development of better prevention and treatment options. Here we show that the Akt inhibitor MK2206 blocks influenza pH1N1 virus infectionin vitro. In particular, at noncytotoxic concentrations, MK2206 alters Akt signaling and inhibits endocytic uptake of the virus. Interestingly, MK2206 is unable to inhibit H3N2, H7N9, and H5N1 viruses, indicating that pH1N1 evolved specific requirements for efficient infection. Thus, Akt signaling could be exploited further for development of better therapeutics against pH1N1 virus.

Cryptosporidiuminfections: molecular advances

Parasitology ◽  
2014 ◽  
Vol 141 (11) ◽  
pp. 1511-1532 ◽  
Author(s):  
MATTHIAS LENDNER ◽  
ARWID DAUGSCHIES
Keyword(s):  
Life Cycle ◽  
Host Cell ◽  
Genetically Modify ◽  
Cell Interaction ◽  
Cell Infection ◽  
Recent Advances ◽  
Host Cell Interaction

SUMMARYCryptosporidiumhost cell interaction remains fairly obscure compared with other apicomplexans such asPlasmodiumorToxoplasma. The reason for this is probably the inability of this parasite to complete its life cyclein vitroand the lack of a system to genetically modifyCryptosporidium. However, there is a substantial set of data about the molecules involved in attachment and invasion and about the host cell pathways involved in actin arrangement that are altered by the parasite. Here we summarize the recent advances in research on host cell infection regarding the excystation process, attachment and invasion, survival in the cell, egress and the available data on omics.

Bacteriophages Associated with Turkey Coecums in Bluecomb-Infected and Healthy Birds

1969 ◽  
Vol 27 ◽  
pp. 226-227
Author(s):  
A. E. Ritchie
Keyword(s):  
Host Cell ◽  
Causal Relationship ◽  
Cell Cultures ◽  
Cell Interaction ◽  
Etiologic Agent ◽  
Viral Origin ◽  
Intestinal Contents ◽  
Host Cell Interaction

The cause of bluecomb disease in turkeys is unknown. Filtration of infective intestinal contents suggests a viral origin. To date, it has not been possible to isolate the etiologic agent in various cell cultures. The purpose of this work was to characterize as many virus-like entities as were recognizable in intestines of both healthy and bluecomb-infected turkeys. By a comparison of the viral populations it was hoped that some insight might be gained into the cause of this disease. Studies of turkey hemorraghic enteritis by Gross and Moore (Avian Dis. 11: 296-307, 1967) have suggested that a bacteriophage-host cell interaction may bear some causal relationship to that disease.

scholarly journals Why Does SARS-CoV-2 Infection Induce Autoantibody Production?

Pathogens ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 380
Author(s):  
Ales Macela ◽  
Klara Kubelkova
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Host Cell ◽  
Critical Role ◽  
Cell Interaction ◽  
Immune Recognition ◽  
Autoantibody Production ◽  
Host Cell Interaction ◽  
Primary Virus

SARS-CoV-2 infection induces the production of autoantibodies, which is significantly associated with complications during hospitalization and a more severe prognosis in COVID-19 patients. Such a response of the patient’s immune system may reflect (1) the dysregulation of the immune response or (2) it may be an attempt to regulate itself in situations where the non-infectious self poses a greater threat than the infectious non-self. Of significance may be the primary virus-host cell interaction where the surface-bound ACE2 ectoenzyme plays a critical role. Here, we present a brief analysis of recent findings concerning the immune recognition of SARS-CoV-2, which, we believe, favors the second possibility as the underlying reason for the production of autoantibodies during COVID-19.

scholarly journals Eosinophil Responses at the Airway Epithelial Barrier during the Early Phase of Influenza a Virus Infection in C57BL/6 Mice

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 509 ◽  
Author(s):  
Meenakshi Tiwary ◽  
Robert J. Rooney ◽  
Swantje Liedmann ◽  
Kim S. LeMessurier ◽  
Amali E. Samarasinghe
Keyword(s):  
Epithelial Cells ◽  
Influenza A Virus ◽  
Early Phase ◽  
Influenza A ◽  
Airway Epithelial Cells ◽  
Epithelial Barrier ◽  
Virus Infectivity ◽  
Airway Epithelial ◽  
In Vivo Models

Eosinophils, previously considered terminally differentiated effector cells, have multifaceted functions in tissues. We previously found that allergic mice with eosinophil-rich inflammation were protected from severe influenza and discovered specialized antiviral effector functions for eosinophils including promoting cellular immunity during influenza. In this study, we hypothesized that eosinophil responses during the early phase of influenza contribute to host protection. Using in vitro and in vivo models, we found that eosinophils were rapidly and dynamically regulated upon influenza A virus (IAV) exposure to gain migratory capabilities to traffic to lymphoid organs after pulmonary infection. Eosinophils were capable of neutralizing virus upon contact and combinations of eosinophil granule proteins reduced virus infectivity through hemagglutinin inactivation. Bi-directional crosstalk between IAV-exposed epithelial cells and eosinophils occurred after IAV infection and cross-regulation promoted barrier responses to improve antiviral defenses in airway epithelial cells. Direct interactions between eosinophils and airway epithelial cells after IAV infection prevented virus-induced cytopathology in airway epithelial cells in vitro, and eosinophil recipient IAV-infected mice also maintained normal airway epithelial cell morphology. Our data suggest that eosinophils are important in the early phase of IAV infection providing immediate protection to the epithelial barrier until adaptive immune responses are deployed during influenza.

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