Akt Inhibitor MK2206 Prevents Influenza pH1N1 Virus InfectionIn Vitro

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.

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

Memórias do Instituto Oswaldo Cruz ◽

10.1590/s0074-02761993000200010 ◽

1993 ◽

Vol 88 (2) ◽

pp. 235-241 ◽

Cited By ~ 2

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

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

International Journal of Molecular Sciences ◽

10.3390/ijms20051101 ◽

2019 ◽

Vol 20 (5) ◽

pp. 1101 ◽

Cited By ~ 14

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.

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

10.20944/preprints202107.0246.v1 ◽

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.

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

10.1101/2021.07.11.451833 ◽

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.

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Cryptosporidiuminfections: molecular advances

Parasitology ◽

10.1017/s0031182014000237 ◽

2014 ◽

Vol 141 (11) ◽

pp. 1511-1532 ◽

Cited By ~ 32

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.

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

Viruses ◽

10.3390/v13081537 ◽

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.

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

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100063044 ◽

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.

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

Pathogens ◽

10.3390/pathogens10030380 ◽

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.

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