scholarly journals NQO2 is differentially expressed in the blood of patients with coronavirus co-infections.

2020 ◽  
Author(s):  
Shahan Mamoor

The human coronavirus SARS-CoV-2 (1) has resulted in the death of over 180,000 Americans in less than one year (2). Infection of a person already suffering from a viral infection, a phenomena known as co-infection can potentially pose a problem during the upcoming influenza seasons. We mined published microarray data (3) to identify genes most differentially expressed in the whole blood of patients suffering from human coronavirus co-infections. We found that the gene encoding NQO2 (4) was among those whose expression changed most significantly transcriptome-wide when comparing the blood of patients suffering from three different types of co-infections: human coronavirus NL63 and rhinovirus, human coronavirus HKU1 and rhinovirus, as well as in human coronavirus 229E and influenza A co-infection. NQO2 is reported to have functions in the B-lymphocyte response (5) and could be relevant to the process of viral co-infection involving the human coronavirus family.

2020 ◽  
Author(s):  
Shahan Mamoor

The human coronavirus SARS-CoV-2 (1) has resulted in the death of over 200,000 Americans in less than one year (2). Infection of a person already suffering from a viral infection, a phenomena known as co-infection can potentially pose a problem during the upcoming influenza season. We mined published microarray data (3) to identify genes most differentially expressed in the whole blood of patients suffering from human coronavirus co-infections. We found that the gene encoding the HLA complex non-coding RNA HCG4 was among those whose expression changed most significantly transcriptome-wide when comparing the blood of patients suffering from three different types of co-infections: human coronavirus NL63 and rhinovirus, human coronavirus HKU1 and rhinovirus, as well as in human coronavirus OC43 and influenza A co-infection. We previously reported significant transcriptome-wide changes in HLA family gene expression (4), as well as in changes in gene expression of the cathepsins in viral co-infection (5). Together, these data suggest the process of antigen presentation could be altered during viral co-infections involving the human coronaviruses.


2020 ◽  
Author(s):  
Shahan Mamoor

The SARS-CoV-2 pandemic has resulted in close to 1,000,000 deaths worldwide in less than one year (1) with an upcoming influenza season, raising the prospect of complications resulting from co-infections. Our understanding of gene expression in patients with viral co-infection is limited. We mined published microarray data (2) to identify transcriptional features most significantly associated with viral co-infection. We identified the cytokine interleukin-16 as among the most differentially expressed genes in the blood of patients with viral co-infections, including in a patient with co-infection of influenza A and human coronavirus OC43 and in a patient with co-infection of influenza A and human coronavirus 229E. Interleukin-16 may be relevant to the biology of viral co-infection.


2020 ◽  
Author(s):  
Shahan Mamoor

The human coronavirus SARS-CoV-2 (1) has resulted in the death of over 200,000 Americans in less than one year (2). Infection of a person already suffering from a viral infection, a phenomena known as co-infection can potentially pose a problem during the upcoming influenza season. We mined published microarray data (3) to identify genes most differentially expressed in the whole blood of patients suffering from viral co-infections, including co-infections involving a human coronavirus. We found that the UVSSA gene, encoding the UV stimulated scaffold protein A, was among the genes whose expression changed most significantly transcriptome-wide when in the blood of four patients suffering from two different types of co-infections: human coronavirus HKU1 and human rhinovirus, as well as in human coronavirus OC43 and influenza A co-infection. UVSSA may be of relevance to biology underlying some viral co-infections.


2020 ◽  
Author(s):  
Shahan Mamoor

Co-infection is defined by the infection of a host or cell by more than one pathogen (1, 2). Infections from the novel coronavirus severe acute respiratory syndrome coronavirus 2, SARS-CoV-2 (3), have resulted in the death of more than 200,000 Americans (4) and over 1,000,000 people worldwide (5) in less than one year. An upcoming influenza season raises the prospect of potential complications arising from co-infections involving SARS-CoV-2 (6). We mined published microarray data (7) to discover transcriptional features of viral co-infection in the blood of human patients. We identified the peptidylglycine alpha-amidating monooxygenase, PAM, as among the genes whose expression was most different in the blood of patients with a variety of viral co-infections, including co-infection of human coronavirus OC43 and influenza A. Transcriptional changes in PAM appeared to be specific to co-infection settings. PAM may be of relevance to fundamental transcriptional biology underlying viral co-infections of human blood.


2020 ◽  
Author(s):  
Shahan Mamoor

Inflammatory bowel diseases (IBD) include Crohn’s Disease and Ulcerative Colitis (1). We mined published microarray data to understand how gene expression in the hematopoietic compartment of patients with Crohn’s Disease is most different from that of healthy controls (2-4). Across two datasets (2, 3), we found that BAFF, also known as the B-lymphocyte stimulator (BLyS), encoded by the gene TNFSF13B (5), was differentially expressed in the blood of patients with Crohn’s Disease . Analysis of a third dataset (4) revealed that BAFF was among the genes most differentially expressed in monocyte-derived macrophages from patients with Crohn’s Disease. Serum BAFF, fecal BAFF, and BAFF expression in the intestinal mucosa has been demonstrated to be increased in patients with IBD (6, 7). We show here that expression of BAFF in the peripheral blood of patients with Crohn’s Disease is also increased.


2020 ◽  
Author(s):  
Shahan Mamoor

The coronavirus COVID19 pandemic is an emerging biosafety threat to the nation and the world (1). There are no treatments approved for coronavirus infection in humans (2) and there is a lack of information available regarding the basic transcriptional behavior of human cells and mammalian tissues following coronavirus infection. We mined independent published (3-5) and public (6) datasets, containing transcriptome data from infection models of the human coronavirus 229E and of severe acute respiratory syndrome (SARS) coronavirus to discover genes that are differentially expressed in coronaviruses and identify potential therapeutic targets and host cell vulnerabilities. We identified IL6 and IL1RN as conserved differentially expressed genes following coronavirus infection. IL6 and IL1RN may be involved in the cellular response to COVID19 infection.


2020 ◽  
Author(s):  
Shahan Mamoor

Non-small cell lung cancer (NSCLC) is the leading cause of cancer death in the United States (1). We mined published microarray data (2, 3, 4, 5) to identify differentially expressed genes in NSCLC. We found that the gene encoding the transcription factor TCF21 was among the genes whose expression was most quantitatively different in tumors from patients with NSCLC as compared to the lung. TCF21 may be important for initiation or progression of non-small cell lung cancer in humans.


2020 ◽  
Author(s):  
Shahan Mamoor

Brain metastases are a clinical problem in patients with breast cancer (1-3). We mined published microarray data (4, 5) to discover genes associated with brain metastasis in patients with brain metastatic breast cancer. We found that the gene encoding the peptide apelin, APLN, was among those most differentially expressed in the brain metastases of patients with brain metastatic breast cancer. APLN may be of relevance to the biology underlying metastasis to the brain in humans with metastatic breast cancer.


2020 ◽  
Author(s):  
Shahan Mamoor

Co-infection is a process by which a cell or organism already infected with a virus is then infected with a second, different virus (1, 2). The human coronavirus SARS-CoV-2 has resulted in the death of nearly 200,000 Americans in less than one year (3, 4); the upcoming influenza could potentially pose a problem with respect to co-infection with Influenza and SARS-CoV-2; significant co-infection in patients with SARS-CoV-2 has been reported (5). We mined a published microarray dataset (6) to discover genes associated with viral co-infection in patients with a coronavirus infection. We found that genes of the HLA family, particularly HLA-DRB and HLA-A, were significantly differentially expressed in the blood of patients with human coronavirus infections, including HCoV-229E, HCoV OC43, HCoV NL63, and HCoV HKU1. Different viral co-infections, including Influenza A, Human Rhinovirus, Enterovirus, and Respiratory Syncytial Virus A co-infections were also associated with significant differential expression of HLA family genes in patient blood. Perturbation of HLA family gene expression appears to be a general feature of viral co-infection in humans.


2005 ◽  
Vol 79 (12) ◽  
pp. 7819-7826 ◽  
Author(s):  
Chung Y. Cheung ◽  
Leo L. M. Poon ◽  
Iris H. Y. Ng ◽  
Winsie Luk ◽  
Sin-Fun Sia ◽  
...  

ABSTRACT The pathogenesis of severe acute respiratory syndrome (SARS) remains unclear. Macrophages are key sentinel cells in the respiratory system, and it is therefore relevant to compare the responses of human macrophages to infections with the SARS coronavirus (SARS-CoV) and other respiratory viruses. Primary human monocyte-derived macrophages were infected with SARS-CoV in vitro. Virus replication was monitored by measuring the levels of positive- and negative-strand RNA, by immunofluorescence detection of the SARS-CoV nucleoprotein, and by titration of the infectious virus. The gene expression profiles of macrophages infected with SARS-CoV, human coronavirus 229E, and influenza A (H1N1) virus were compared by using microarrays and real-time quantitative reverse transcriptase PCR. Secreted cytokines were measured with an enzyme-linked immunosorbent assay. SARS-CoV initiated viral gene transcription and protein synthesis in macrophages, but replication was abortive and no infectious virus was produced. In contrast to the case with human coronavirus 229E and influenza A virus, there was little or no induction of beta interferon (IFN-β) in SARS-CoV-infected macrophages. Furthermore, SARS-CoV induced the expression of chemokines such as CXCL10/IFN-γ-inducible protein 10 and CCL2/monocyte chemotactic protein 1. The poor induction of IFN-β, a key component of innate immunity, and the ability of the virus to induce chemokines could explain aspects of the pathogenesis of SARS.


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