Virus interactions with endothelial cell receptors: implications for viral pathogenesis

Dalrymple, Nadine A.; Mackow, Erich R.

doi:10.1016/j.coviro.2014.06.006

Cited by 53 publications

(52 citation statements)

References 118 publications

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“…High level in viral load of ANDV‐South samples could be related to the person‐to‐person transmission. Highly variable viral load values were observed among cases, suggesting that host–virus interaction could be a factor in HPS pathogenesis as was proposed previously [Dalrymple and Mackow, ; Guichard et al, ; Hepojoki et al, ; Baigildina et al, ].…”

Section: Discussionsupporting

confidence: 64%

Viral load of patients with hantavirus pulmonary syndrome in Argentina

Bellomo

Pires-Marczeski

Padula

2015

Journal of Medical Virology

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Hantavirus causes severe illness including pneumonia, which leads to hospitalization and often death. At present, there is no specific treatment available. The hantavirus pathogenesis is not well understood, but most likely both virus-mediated and host-mediated mechanisms, are involved. The aim of this study was to correlate viral load in samples of hantavirus pulmonary syndrome cases and hantavirus infected individuals, with clinical epidemiological parameters and disease outcome. The variables that could potentially be related with viral load were analyzed. The retrospective study included 73 cases or household contacts, with different clinical evolution. Viral load was measured by reverse-transcription and real time polymerase chain reaction. There was no statistically significant association between blood viral RNA levels and severity of disease. However, viral load was inversely correlated with IgG response in a statistically significant manner. The level of viral RNA was significantly higher in patients infected with Andes virus South lineage, and was markedly low in persons infected with Laguna Negra virus. These results suggest that the infecting viral genotype is associated with disease severity, and that high viral load is associated with a low specific IgG response. Sex, age and disease severity were not related with viral load. Further investigations increasing strikingly the number of cases and also limiting the variables to be studied are necessary.

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Section: Discussionsupporting

confidence: 64%

Viral load of patients with hantavirus pulmonary syndrome in Argentina

Bellomo

Pires-Marczeski

Padula

2015

Journal of Medical Virology

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“…It has been shown that human endothelial cells are highly susceptible to dengue virus infection (56). Uninfected endothelial cells might also participate in the disease process via complement receptors on endothelial cells and platelets that can mediate inflammatory responses (5758); however, the infected endothelium, in the presence of cross-reactive antibodies, might resemble the endothelium of a host experiencing graft rejection (59). ADE by itself is not thought to correlate with disease severity and DHF; complement activation by virus-antibody or antigen-antibody complexes is a feature of severe dengue infection, and it is temporally related to plasma leakage (6).…”

Section: Original Antigenic Sin and Dengue Virus Infection: Classic 'mentioning

confidence: 99%

Original Antigenic Sin Response to RNA Viruses and Antiviral Immunity

et al. 2016

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The human immune system has evolved to fight against foreign pathogens. It plays a central role in the body's defense mechanism. However, the immune memory geared to fight off a previously recognized pathogen, tends to remember an original form of the pathogen when a variant form subsequently invades. This has been termed 'original antigenic sin'. This adverse immunological effect can alter vaccine effectiveness and sometimes cause enhanced pathogenicity or additional inflammatory responses, according to the type of pathogen and the circumstances of infection. Here we aim to give a simplified conceptual understanding of virus infection and original antigenic sin by comparing and contrasting the two examples of recurring infections such as influenza and dengue viruses in humans.

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“…A number of cytokines such as IL‐6, IL‐8 and IFNs are elicited in response to infection . A focus of many dengue researchers is to understand altered endothelial function by immune activators and DENV products and identify important contributors to the plasma leakage seen in DHF …”

Section: Introductionmentioning

confidence: 99%

Upregulation of HLA‐E by dengue and not Zika viruses

et al. 2018

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IntroductionThe most severe form of dengue virus (DENV) illness, dengue haemorrhagic fever, is characterised by plasma leakage and increased vascular permeability.ObjectivesGiven the critical role that endothelial cells play in the pathogenesis of DENV, we wanted to determine whether infection with DENV altered the expression of MHC class I related genes including HLA‐E.ResultsIn this study, we provide evidence that HLA‐E but not MICA/B or HLA‐G is upregulated by all four serotypes of DENV in an endothelial cell line human microvascular endothelial cells (HMEC)‐1. In contrast, Zika virus (ZIKV), a related flavivirus, where plasma leakage is not a major manifestation of disease, did not upregulate HLA‐E. We found modest levels of soluble HLA‐E in supernatants from DENV but not ZIKV‐infected cells. Coculture experiments found minimal activation of natural killer (NK) cells in the presence of both uninfected and infected HMEC‐1 cells. HLA‐E induced by DENV infection could not dampen the degranulation of activated NK cells by interacting with its ligand NKG2a.ConclusionsOur results suggest that while DENV infection induces HLA‐E, the high MHC class I expression on uninfected and infected HMEC‐1 cells may dominate the diverse signals generated between inhibitory and activating receptors on NK cells and ligands on target cells.

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Virus interactions with endothelial cell receptors: implications for viral pathogenesis

Cited by 53 publications

References 118 publications

Viral load of patients with hantavirus pulmonary syndrome in Argentina

Viral load of patients with hantavirus pulmonary syndrome in Argentina

Original Antigenic Sin Response to RNA Viruses and Antiviral Immunity

Upregulation of HLA‐E by dengue and not Zika viruses

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