Gene expression profiles in peripheral blood mononuclear cells of SARS patients

Yu, Shi Yan; Hu, Yun Wen; Liu, Xiao Ying; Xiong, Wei; Zhou, Zhi Tong; Yuan, Zheng

doi:10.3748/wjg.v11.i32.5037

Cited by 48 publications

(49 citation statements)

References 30 publications

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“…In agreement with the above consideration, it has been reported that several IFN-stimulated genes, such as PKR, GBP-1/2, CXL-10/11, and JAK/STAT signal pathway were down-regulated in SARS patients with acute severe phase compared to patients with the convalescent phase [11] .…”

supporting

confidence: 68%

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Severe Acute Respiratory Syndrome Coronavirus Elicits a Weak Interferon Response Compared to Traditional Interferon-Inducing Viruses

et al. 2008

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The aim of the present study is to investigate changes of interferon (IFN) production occurring over the first 48 h after infection of peripheral blood mononuclear cells (PBMCs) with severe acute respiratory syndrome (SARS) coronavirus (CoV) and to compare these changes to those induced by well-established IFN-inducing viruses, such as vesicular stomatitis (VSV) and Newcastle viruses (NDV). Experiments have been carried out using PBMCs of 10 different healthy donors. The results showed that the antiviral activity of IFN contained in the supernatant of SARS-CoV-infected PBMCs was lower than those induced by VSV and NDV. Consequently, SARS-CoV induces a lower synthesis of IFN-α, -β and -γ compared to VSV and NDV. Characterization of the profile of IFN-α subtypes genes expression in SARS-CoV-infected PBMCs demonstrated that the level of IFN-α2 and -6 subtypes were higher compared to other IFN-α subtypes namely, IFN-α5, -8, -10, -13/1, -17, and -21. In conclusion, SARS-CoV induces IFNs to a less extent compared to VSV and NDV, thus suggesting that the IFN system does play a limited role in early host defense against SARS-CoV infection.

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supporting

confidence: 68%

“…Altogether, the data presented in this study, along with previous results [10][11][12][13][14][15][16][17][18][19] , demonstrate that SARS-CoV is a weak inducer of IFN-␣ , -␤ and -␥ . The potential limitations of our study include the fact that we did not compare IFN response in SARS-CoV-infected PBMCs with those in other relevant human virus.…”

mentioning

confidence: 61%

Severe Acute Respiratory Syndrome Coronavirus Elicits a Weak Interferon Response Compared to Traditional Interferon-Inducing Viruses

et al. 2008

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“…Most studies that use tissue or blood samples from SARS patients did not find a strong interferon response in these patients [15–17,38,39]. This apparent absence of interferon induction in human SARS patients can be explained by the fact that good quality tissue and blood samples from SARS patients were not readily available and even more by the fact that samples were often taken at the time of death, for example, late during infection, making type-I interferon levels difficult to detect.…”

Section: Interferon Induction By Sars-covmentioning

confidence: 99%

Unraveling the Complexities of the Interferon Response During Sars-Cov Infection

et al. 2008

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Viruses employ different strategies to circumvent the antiviral actions of the innate immune response. SARS coronavirus (SARS-CoV), a virus that causes severe lung damage, encodes an array of proteins able to inhibit induction and signaling of type-I interferons. However, recent studies have demonstrated that interferons are produced during SARS-CoV infection in humans and macaques. Furthermore, nuclear translocation of activated STAT1 and a range of interferon-stimulated genes could be demonstrated in the lungs of SARS-CoV-infected macaques. In line with these observations, plasmacytoid dendritic cells have been shown to produce interferons upon SARS-CoV infection in vitro. Given the pivotal role of interferons during viral infections, (differential) induction of interferons may affect the outcome of the infection. Therefore, the functional implication of interferon production during SARS-CoV infection remains to be re-investigated. Rapid spread of the virus owing to air travel, immediate media coverage all over the world and the globalization of the economy contributed to the high impact of the epidemic. The emergence of this new highly pathogenic virus led to a quick response from the scientific world; only a few months after the first emergence of SARS, a newly discovered coronavirus (CoV) was identified as its etiological agent [1][2][3][4]. Many of the people that were infected with SARS-CoV early during the epidemic had been in close contact with live animals on Chinese wet markets, suggesting that the virus came from an animal source [5]. The current hypothesis is that bats are the main natural reservoirs of SARS-CoV-like viruses, and virus transmission to humans most likely occurred via civet cats, which are common trade animals on these wet markets [6]. KeywordsInfection with SARS-CoV in humans initially causes lower respiratory tract disease with clinical symptoms that include fever, malaise and lymphopenia [7][8][9][10]. Approximately 20-30% of SARS patients suffered from severe disease and needed to be transferred to intensive care units. Ultimately, the overall fatality rate approached 10-20% in adults, while children seemed to be relatively resistant to SARS [11]. The clinical course of SARS follows three phases. The first phase is characterized by active viral replication and patients experience the first symptoms of disease, such as fever and malaise. Virus levels start to decrease while antibodies, which are effective in controlling infection, increase in the second phase. Nonetheless, pneumonia and immunopathological injury also develop in this phase. Eventually, in the third phase, fatal cases of SARS develop severe pneumonia and acute respiratory distress syndrome (ARDS), characterized by the presence of diffuse alveolar damage [7]. Although a wide range of animal species are susceptible to experimental infection with SARS-CoV, nonhuman primates are the only animals in which pathology similar to that of human SARS patients has been observed so far. ARDS is characterized by massive in...

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“…Several studies have shown that peripheral-blood mononuclear cells (PBMCs) from SARS-CoV-infected individuals produce high amounts of inflammatory cytokines and chemokines, but not type I IFNs. [22][23][24] Furthermore, in vitro studies have shown that neither macrophages nor monocyte-derived DCs respond to SARS-CoV infection with significant IFN-␣ production. [25][26][27][28] Nonetheless, there is clear evidence that treatment with recombinant IFN-␤ or IFN-␣ can inhibit SARS-CoV replication in vitro, [29][30][31] and, most importantly, diminish the severity of SARS-CoV infection in vivo.…”

mentioning

confidence: 99%

Control of coronavirus infection through plasmacytoid dendritic-cell–derived type I interferon

Cervantes-Barragán

Züst

Weber³

et al. 2006

Blood

370

428

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This study demonstrates a unique and crucial role of plasmacytoid dendritic cells (pDCs) and pDC-derived type I interferons (IFNs) in the pathogenesis of mouse coronavirus infection. pDCs controlled the fast replicating mouse hepatitis virus (MHV) through the immediate production of type I IFNs. Recognition of MHV by pDCs was mediated via TLR7 ensuring a swift IFN-alpha production following encounter with this cytopathic RNA virus. Furthermore, the particular type I IFN response pattern was not restricted to the murine coronavirus, but was also found in infection with the highly cytopathic human severe acute respiratory syndrome (SARS) coronavirus. Taken together, our results suggest that rapid production of type I IFNs by pDCs is essential for the control of potentially lethal coronavirus infections.

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Gene expression profiles in peripheral blood mononuclear cells of SARS patients

Abstract: Gene expression in SARS patients mirrors a host state of inflammation and anti-viral immunity at the transcription level, and understanding of gene expression profiles may make contribution to further studies of the SARS pathogenesis.

Cited by 48 publications

References 30 publications

Severe Acute Respiratory Syndrome Coronavirus Elicits a Weak Interferon Response Compared to Traditional Interferon-Inducing Viruses

Severe Acute Respiratory Syndrome Coronavirus Elicits a Weak Interferon Response Compared to Traditional Interferon-Inducing Viruses

Unraveling the Complexities of the Interferon Response During Sars-Cov Infection

Control of coronavirus infection through plasmacytoid dendritic-cell–derived type I interferon

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