Serum Concentrations of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor, Nitric Oxide and Endothelial DNA Proliferation in Development of Microvascular Pathology in Acute African Swine Fever

Tatoyan, M.R.; Ter-Pogossyan, Z.R.; Semerjyan, Anna; Gevorgyan, Vardan; Karalyan, N.; Sahakyan, Carmen T.; Mkrtchyan, G.L.; Gazaryan, H.K.; Avagyan, Hranush; Karalyan, Zaven

doi:10.1016/j.jcpa.2018.12.004

Cited by 6 publications

(6 citation statements)

References 42 publications

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“…Such an increase came later than the increase of VEGFB plasma levels and was detected once vascular damage and hemorrhages were already present in infected pigs. It was suggested that CXCL12 release could be a compensatory mechanism to counteract the increased vascular permeability at final stages of the disease [ 101 ].…”

Section: Circulating Levels Of Cytokines During Asfv Infection In Vivomentioning

confidence: 99%

African Swine Fever Virus Infection and Cytokine Response In Vivo: An Update

Franzoni

Pedrera

Sánchez-Cordón

2023

Viruses

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African swine fever (ASF) is a hemorrhagic viral disease of domestic pigs and wild suids (all Sus scrofa) caused by the ASF virus (ASFV). The disease is spreading worldwide without control, threatening pig production due to the absence of licensed vaccine or commercially available treatments. A thorough understanding of the immunopathogenic mechanisms behind ASFV infection is required to better fight the disease. Cytokines are small, non-structural proteins, which play a crucial role in many aspects of the immune responses to viruses, including ASFV. Infection with virulent ASFV isolates often results in exacerbated immune responses, with increased levels of serum pro-inflammatory interleukins (IL-1α, IL-1β, IL-6), TNF and chemokines (CCL2, CCL5, CXCL10). Increased levels of IL-1, IL-6 and TNF are often detected in several tissues during acute ASFV infections and associated with lymphoid depletion, hemorrhages and oedemas. IL-1Ra is frequently released during ASFV infection to block further IL-1 activity, with its implication in ASFV immunopathology having been suggested. Increased levels of IFN-α and of the anti-inflammatory IL-10 seem to be negatively correlated with animal survival, whereas some correlation between virus-specific IFN-γ-producing cells and protection has been suggested in different studies where different vaccine candidates were tested, although future works should elucidate whether IFN-γ release by specific cell types is related to protection or disease development.

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Section: Circulating Levels Of Cytokines During Asfv Infection In Vivomentioning

confidence: 99%

African Swine Fever Virus Infection and Cytokine Response In Vivo: An Update

Franzoni

Pedrera

Sánchez-Cordón

2023

Viruses

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“…This has been shown both in vitro and in vivo. The increase in DNA content in various cells and tissues in the acute form of ASF, which was previously discussed by us [ 14 , 28 ]. In animals, it is undoubtedly associated with viremia, which is observed by the end of day 1 after infection with virulent strains of the virus and, consequently, results in the infection of internal organs.…”

Section: Discussionmentioning

confidence: 71%

“…In our previous works it was shown that the PAM entered the S phase and started DNA synthesis upon exposure to the ASF virus [ 28 ]. To study cellular proteins, we measured the levels of cyclin A and E in PAM lysates.…”

Section: Resultsmentioning

confidence: 99%

African Swine Fever Virus Manipulates the Cell Cycle of G0-Infected Cells to Access Cellular Nucleotides

Avagyan

Hakobyan

Poghosyan

et al. 2022

Viruses

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African swine fever virus manipulates the cell cycle of infected G0 cells by inducing its progression via unblocking cells from the G0 to S phase and then arresting them in the G2 phase. DNA synthesis in infected alveolar macrophages starts at 10–12 h post infection. DNA synthesis in the nuclei of G0 cells is preceded by the activation of the viral genes K196R, A240L, E165R, F334L, F778R, and R298L involved in the synthesis of nucleotides and the regulation of the cell cycle. The activation of these genes in actively replicating cells begins later and is less pronounced. The subsequent cell cycle arrest at the G2 phase is also due to the cessation of the synthesis of cellular factors that control the progression of the cell cycle–cyclins. This data describes the manipulation of the cell cycle by the virus to gain access to the nucleotides synthesized by the cell. The genes affecting the cell cycle simply remain disabled until the beginning of cellular DNA synthesis (8–9 hpi). The genes responsible for the synthesis of nucleotides are turned on later in the presence of nucleotides and their transcriptional activity is lower than that during virus replication in an environment without nucleotides.

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“…It will be of particular interest to determine which viral genes shape the innate immune response to ASFV, and how this process leads to endothelial dysfunction and cytokine storm, the main hallmarks of virulent ASFV infection ( Figure 1 ). While direct infection of endothelial cells has been reported to trigger apoptosis ( Vallée et al, 2001 ), endothelial dysfunction may also be an indirect consequence of excessive proinflammatory cytokine production ( Tatoyan et al, 2019 ). Further studies may also shed light on the mechanisms responsible for the lack of virulence of some naturally attenuated ASFV strains in domestic pigs, as well as for ASFV persistence in wild African suids, which do not develop symptoms upon infection ( Oura et al, 1998 ).…”

Section: Discussionmentioning

confidence: 99%

New Insights in the Interplay Between African Swine Fever Virus and Innate Immunity and Its Impact on Viral Pathogenicity

et al. 2022

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The continuous spread of African swine fever virus (ASFV) in Europe and Asia represents a major threat to livestock health, with billions of dollars of income losses and major perturbations of the global pig industry. One striking feature of African swine fever (ASF) is the existence of different forms of the disease, ranging from acute with mortality rates approaching 100% to chronic, with mild clinical manifestations. These differences in pathogenicity have been linked to genomic alterations present in attenuated ASFV strains (and absent in virulent ones) and differences in the immune response of infected animals. In this mini-review, we summarized current knowledge on the connection between ASFV pathogenicity and the innate immune response induced in infected hosts, with a particular focus on the pathways involved in ASFV detection. Indeed, recent studies have highlighted the key role of the DNA sensor cGAS in ASFV sensing. We discussed what other pathways may be involved in ASFV sensing and inflammasome activation and summarized recent findings on the viral ASFV genes involved in the modulation of the interferon (IFN) and nuclear factor kappa B (NF-κB) pathways.

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Serum Concentrations of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor, Nitric Oxide and Endothelial DNA Proliferation in Development of Microvascular Pathology in Acute African Swine Fever

Cited by 6 publications

References 42 publications

African Swine Fever Virus Infection and Cytokine Response In Vivo: An Update

African Swine Fever Virus Infection and Cytokine Response In Vivo: An Update

African Swine Fever Virus Manipulates the Cell Cycle of G0-Infected Cells to Access Cellular Nucleotides

New Insights in the Interplay Between African Swine Fever Virus and Innate Immunity and Its Impact on Viral Pathogenicity

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