Altered cytokine levels and immune responses in patients with SARS-CoV-2 infection and related conditions

Noroozi, Rezvan; Branicki, Wojciech; Pyrć, Krzysztof; Łabaj, Paweł P.; Pośpiech, Ewelina; Taheri, Mohammad; Ghafouri‐Fard, Soudeh

doi:10.1016/j.cyto.2020.155143

Cited by 71 publications

(65 citation statements)

References 32 publications

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“…1a), of which upregulation were also reported in the COVID-19 patients. 13 Furthermore, SARS-CoV-2 infection of Calu-3 cells induced IL-1β processing and secretion in an multiplicity of infection (MOI)-dependent manner (Fig. 1b).…”

Section: Sars-cov-2 Infection Induces Inflammatory Responses In Lungmentioning

confidence: 89%

SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation

Zhang

Guan

et al. 2020

Sig Transduct Target Ther

317

346

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can lead to respiratory illness and multi-organ failure in critically ill patients. Although the virus-induced lung damage and inflammatory cytokine storm are believed to be directly associated with coronavirus disease 2019 (COVID-19) clinical manifestations, the underlying mechanisms of virus-triggered inflammatory responses are currently unknown. Here we report that SARS-CoV-2 infection activates caspase-8 to trigger cell apoptosis and inflammatory cytokine processing in the lung epithelial cells. The processed inflammatory cytokines are released through the virus-induced necroptosis pathway. Virus-induced apoptosis, necroptosis, and inflammation activation were also observed in the lung sections of SARS-CoV-2-infected HFH4-hACE2 transgenic mouse model, a valid model for studying SARS-CoV-2 pathogenesis. Furthermore, analysis of the postmortem lung sections of fatal COVID-19 patients revealed not only apoptosis and necroptosis but also massive inflammatory cell infiltration, necrotic cell debris, and pulmonary interstitial fibrosis, typical of immune pathogenesis in the lung. The SARS-CoV-2 infection triggered a dual mode of cell death pathways and caspase-8-dependent inflammatory responses may lead to the lung damage in the COVID-19 patients. These discoveries might assist the development of therapeutic strategies to treat COVID-19.

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Section: Sars-cov-2 Infection Induces Inflammatory Responses In Lungmentioning

confidence: 89%

SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation

Zhang

Guan

et al. 2020

Sig Transduct Target Ther

317

346

View full text Add to dashboard Cite

show abstract

“…IgA response is also much stronger and persistent than IgM response (11). However, in some patients, a defective immune response results due to the overproduction of pro-inflammatory cytokines leading to cytokine storm (12). A higher level of cytokines leading to inflammation in multiple organs has been observed in intensive care unit (ICU) patients than in non-ICU patients (13).…”

Section: Immunological Response To Sars-cov-2 and Cytokine Stormmentioning

confidence: 99%

Single Virus Targeting Multiple Organs: What We Know and Where We Are Heading?

Prasad

2020

Front. Med.

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COVID-19 caused by SARS-CoV-2 has already infected more than 6. 3 million people worldwide as of 1st June 2020 and caused a global medical emergency. Healthcare professionals have been struggling to devise appropriate therapeutic strategies against the virus mainly due to the diverse range of symptoms and multiple-organ failure in infected patients. Several broad-spectrum antiviral drugs are being used for treatment; however, there is yet no specific drug or vaccine against the virus. Multiple-organ failure due to hyperactivity of the immune system resulting in cytokine storms is a major reason for death among the 5% critically ill patients. In this article, we have discussed the damage caused by COVID-19 on different organs of the human body.

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“… 5 Moreover, higher plasma levels of IL-2, IL-7, IL-10, GCSF, IP-10, MCP-1, MIP-1A, and TNF-α were reported in ICU COVID-19 patients with severe disease. 5 , 272 SARS-CoV-2 infection activates an inflammatory response that plays an antiviral role, but overproduction of cytokine occurs when there is a loss of negative feedback. This unbalanced feedback recruits more immune cells to the site of infection, leading to organ damage.…”

Section: Pro-inflammatory Cytokinesmentioning

confidence: 99%

Targeting Crucial Host Factors of SARS-CoV-2

et al. 2020

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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide since its first incidence in Wuhan, China, in December 2019. Although the case fatality rate of COVID-19 appears to be lower than that of SARS and Middle East respiratory syndrome (MERS), the higher transmissibility of SARS-CoV-2 has caused the total fatality to surpass other viral diseases, reaching more than 1 million globally as of October 6, 2020. The rate at which the disease is spreading calls for a therapy that is useful for treating a large population. Multiple intersecting viral and host factor targets involved in the life cycle of the virus are being explored. Because of the frequent mutations, many coronaviruses gain zoonotic potential, which is dependent on the presence of cell receptors and proteases, and therefore the targeting of the viral proteins has some drawbacks, as strain-specific drug resistance can occur. Moreover, the limited number of proteins in a virus makes the number of available targets small. Although SARS-CoV and SARS-CoV-2 share common mechanisms of entry and replication, there are substantial differences in viral proteins such as the spike (S) protein. In contrast, targeting cellular factors may result in a broader range of therapies, reducing the chances of developing drug resistance. In this Review, we discuss the role of primary host factors such as the cell receptor angiotensin-converting enzyme 2 (ACE2), cellular proteases of S protein priming, post-translational modifiers, kinases, inflammatory cells, and their pharmacological intervention in the infection of SARS-CoV-2 and related viruses.

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Altered cytokine levels and immune responses in patients with SARS-CoV-2 infection and related conditions

Cited by 71 publications

References 32 publications

SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation

SARS-CoV-2 triggers inflammatory responses and cell death through caspase-8 activation

Single Virus Targeting Multiple Organs: What We Know and Where We Are Heading?

Targeting Crucial Host Factors of SARS-CoV-2

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