Case Report: Death due to COVID-19 in Three Brothers

Yousefzadegan, Sedigheh; Rezaei, Nima

doi:10.4269/ajtmh.20-0240

Cited by 69 publications

(49 citation statements)

References 3 publications

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“…This evidence is in keeping with the key role of IFNλs in the response to viral infection sustained by negative- and positive-sense RNA virus, double stranded RNA viruses and DNA viruses. As proof of the key role of type III IFNs in the regulation of immunity response, single nucleotide polymorphisms in IFNλ genes were strongly associated with outcomes of viral infection [ 10 ]. Between them, the rs1297860(C/T) located ~3 kb upstream of IFNL3 and the frame shift variant rs368234815 (TT/ΔG), which are in high linkage disequilibrium, represent the strongest host factor associated with viral clearance.…”

Section: Discussionmentioning

confidence: 99%

“…A possible contribution of human gene polymorphisms involved in the host antiviral responses to SARS-CoV-2 has been recently postulated, and there is growing evidence that some gene polymorphisms could affect susceptibility and severity of the COVID-19 course [ 7 ]. Family clustering of severe cases has been reported worldwide, which supports further efforts in exploring these genetic determinants in order to be better prepared for future waves [ 8 , 9 , 10 ].…”

Section: Introductionmentioning

confidence: 90%

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SARS-CoV-2 Viral Load, IFNλ Polymorphisms and the Course of COVID-19: An Observational Study

Amodio

Pipitone

Grimaudo

et al. 2020

JCM

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The course of SARS-CoV-2 infection ranges from asymptomatic to a multiorgan disease. In this observational study, we investigated SARS-CoV-2 infected subjects with defined outcomes, evaluating the relationship between viral load and single nucleotide polymorphisms of genes codifying for IFNλs (interferon). The study enrolled 381 patients with laboratory-confirmed SARS-CoV-2 infection. For each patient, a standardized form was filled including sociodemographic variables and clinical outcomes. The host’s gene polymorphisms (IFNL3 rs1297860 C/T and INFL4 rs368234815 TT/ΔG) and RtReal-Time PCR cycle threshold (PCR Ct) value on SARS-CoV-2 were assessed on nasal, pharyngeal or nasopharyngeal swabs. Higher viral loads were found in patients aged > 74 years and homozygous mutant polymorphisms DG in IFNL4 (adj-OR = 1.16, 95% CI = 1.01–1.34 and adj-OR = 1.24, 95% CI = 1.09–1.40, respectively). After adjusting for age and sex, a statistically significantly lower risk of hospitalization was observed in subjects with higher RtReal-Time PCR cycle threshold values (adj-OR = 0.95, 95% CI = 0.91, 0.99; p = 0.028). Our data support the correlation between SARS-CoV-2 load and disease severity, and suggest that IFNλ polymorphisms could affect the ability of the host to modulate viral infection without a clear impact on the outcome of COVID-19.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 90%

SARS-CoV-2 Viral Load, IFNλ Polymorphisms and the Course of COVID-19: An Observational Study

Amodio

Pipitone

Grimaudo

et al. 2020

JCM

View full text Add to dashboard Cite

show abstract

“…Older people and people with comorbidity, especially cardiovascular disease, diabetes, mostly make up the population of those dying from COVID-19 (Ahmadi et al 2020;Hessami et al 2020;Shamshirian and Rezaei 2020;Sahu et al 2020). However, the observation of severe infection and death from infection in young people and people without a preexisting condition has pointed to the possible role of genetics in susceptibility to COVID-19 (Ahanchian et al 2020;Darbeheshti and Rezaei 2020;Yousefzadegan and Rezaei 2020).…”

Section: Introductionmentioning

confidence: 99%

Anosmia: a missing link in the neuroimmunology of coronavirus disease 2019 (COVID-19)

Yazdanpanah

Saghazadeh

Rezaei

2020

Reviews in the Neurosciences

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Just before 2020 began, a novel coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), brought for humans a potentially fatal disease known as coronavirus disease 2019 (COVID-19). The world has thoroughly been affected by COVID-19, while there has been little progress towards understanding the pathogenesis of COVID-19. Patients with a severe phenotype of disease and those who died from the disease have shown hyperinflammation and were more likely to develop neurological manifestations, linking the clinical disease with neuroimmunological features. Anosmia frequently occurs early in the course of COVID-19. The prevalence of anosmia would be influenced by self-diagnosis as well as self-misdiagnosis in patients with COVID-19. Despite this, the association between anosmia and COVID-19 has been a hope for research, aiming to understand the pathogenesis of COVID-19. Studies have suggested differently probable mechanisms for the development of anosmia in COVID-19, including olfactory cleft syndrome, postviral anosmia syndrome, cytokine storm, direct damage of olfactory sensory neurons, and impairment of the olfactory perception center in the brain. Thus, the observation of anosmia would direct us to find the pathogenesis of COVID-19 in the central nervous system, and this is consistent with numerous neurological manifestations related to COVID-19. Like other neurotropic viruses, SARS-CoV-2 might be able to enter the central nervous system via the olfactory epithelium and induce innate immune responses at the site of entry. Viral replication in the nonneural olfactory cells indirectly causes damage to the olfactory receptor nerves, and as a consequence, anosmia occurs. Further studies are required to investigate the neuroimmunology of COVID-19 in relation to anosmia.

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“…Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), responsible for the global pandemic, has brought the whole world to a stand-still 1,2 . The contagious nature of this virus is concerning as it has infected more than 25 million people worldwide claiming 850,000 deaths, so far [3][4][5] . In addition to low-pathogenicity and endemic coronaviruses, high pathogenic Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) and Middle East Respiratory Syndrome Coronavirus (MERS-CoV) in 2002 and 2013, respectively, caused severe human illnesses, e.g.…”

Section: Introductionmentioning

confidence: 99%

Notable sequence homology of the ORF10 protein introspects the architecture of SARS-COV-2

Hassan¹,

Attrish

Ghosh

et al. 2020

Preprint

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The global public health is endangered due to COVID-19 pandemic, which is caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). Despite having similar pathology to MERS and SARS-CoV, the infection fatality rate of SARS-CoV-2 is likely lower than 1%. SARS-CoV-2 has been reported to be uniquely characterized by the accessory protein ORF10, which contains eleven cytotoxic T lymphocyte (CTL) epitopes of nine amino acids length each, across various human leukocyte antigen (HLA) subtypes. In this study, all missense mutations found in sequence databases were examined across twnety-two unique SARS-CoV-2 ORF10 variants that could possibly alter viral pathogenicity. Some of these mutations decrease the stability of ORF10, e.g. I4L and V6I were found in the MoRF region of ORF10 which may also possibly contribute to Intrinsic protein disorder. Furthermore, a physicochemical and structural comparative analysis was carried out on SARS-CoV-2 and Pangolin-CoV ORF10 proteins, which share 97.37% amino acid homology. The high degree of physicochemical and structural similarity of ORF10 proteins of SARS-CoV-2 and Pangolin-CoV open questions about the architecture of SARS-CoV-2 due to the disagreement of these two ORF10 proteins over their sub-structure (loop/coil region), solubility, antigenicity and change from the strand to coil at amino acid position 26, where tyrosine is present. Altogether, SARS-CoV-2 ORF10 is a promising pharmaceutical target and a protein which should be monitored for changes which correlate to change pathogenesis and clinical course of COVID-19 infection.

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Case Report: Death due to COVID-19 in Three Brothers

Cited by 69 publications

References 3 publications

SARS-CoV-2 Viral Load, IFNλ Polymorphisms and the Course of COVID-19: An Observational Study

SARS-CoV-2 Viral Load, IFNλ Polymorphisms and the Course of COVID-19: An Observational Study

Anosmia: a missing link in the neuroimmunology of coronavirus disease 2019 (COVID-19)

Notable sequence homology of the ORF10 protein introspects the architecture of SARS-COV-2

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