Pro-inflammatory CXCL-10, TNF-α, IL-1β, and IL-6: biomarkers of SARS-CoV-2 infection
Currently, the world is witnessing the pandemic of COVID-19, a disease caused by the novel coronavirus SARS-CoV-2. Reported differences in clinical manifestations and outcomes in SARS-CoV-2 infection could be attributed to factors such as virus replication, infiltration of inflammatory cells, and al...
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| Veröffentlicht in: | Archives of virology 2021-12, Vol.166 (12), p.3301-3310 |
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| creator | Tripathy, Anuradha S. Vishwakarma, Siddhesh Trimbake, Diptee Gurav, Yogesh K. Potdar, Varsha A. Mokashi, Nitin D. Patsute, Sudhir D. Kaushal, Himanshu Choudhary, Manohar L. Tilekar, Bipin N. Sarje, Prakash Dange, Varsha S. Abraham, Priya |
| description | Currently, the world is witnessing the pandemic of COVID-19, a disease caused by the novel coronavirus SARS-CoV-2. Reported differences in clinical manifestations and outcomes in SARS-CoV-2 infection could be attributed to factors such as virus replication, infiltration of inflammatory cells, and altered cytokine production. Virus-induced aberrant and excessive cytokine production has been linked to the morbidity and mortality of several viral infections. Using a Luminex platform, we investigated plasma cytokine and chemokine levels of 27 analytes from hospitalized asymptomatic (
n
= 39) and mildly symptomatic (
n
= 35) SARS-CoV-2-infected patients (in the early phase of infection), recovered individuals (45-60 days postinfection) (
n
= 40), and uninfected controls (
n
= 36) from the city of Pune located in the state of Maharashtra in India. Levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α and the chemokine CXCL-10 were significantly higher, while those of the antiviral cytokines IFN-γ and IL-12 p70 were significantly lower in both asymptomatic and mildly symptomatic patients than in controls. Comparison among the patient categories revealed no difference in the levels of the cytokines/chemokines except for CXCL-10 being significantly higher and IL-17, IL-4, and VEGF being significantly lower in the mildly symptomatic patients. Interestingly, levels of all key analytes were significantly lower in recovered individuals than in those in both patient categories. Nevertheless, the level of CXCL10 was significantly higher in the recovered patients than in the controls, indicating that the immune system of SARS-CoV-2 patients may take a longer time to normalize. Our data suggest that IL-6, IL-1β, TNF-α, CXCL-10, and reduced antiviral cytokines could be used as biomarkers of SARS-CoV-2 infection. |
| doi_str_mv | 10.1007/s00705-021-05247-z |
| format | Article |
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n
= 39) and mildly symptomatic (
n
= 35) SARS-CoV-2-infected patients (in the early phase of infection), recovered individuals (45-60 days postinfection) (
n
= 40), and uninfected controls (
n
= 36) from the city of Pune located in the state of Maharashtra in India. Levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α and the chemokine CXCL-10 were significantly higher, while those of the antiviral cytokines IFN-γ and IL-12 p70 were significantly lower in both asymptomatic and mildly symptomatic patients than in controls. Comparison among the patient categories revealed no difference in the levels of the cytokines/chemokines except for CXCL-10 being significantly higher and IL-17, IL-4, and VEGF being significantly lower in the mildly symptomatic patients. Interestingly, levels of all key analytes were significantly lower in recovered individuals than in those in both patient categories. Nevertheless, the level of CXCL10 was significantly higher in the recovered patients than in the controls, indicating that the immune system of SARS-CoV-2 patients may take a longer time to normalize. Our data suggest that IL-6, IL-1β, TNF-α, CXCL-10, and reduced antiviral cytokines could be used as biomarkers of SARS-CoV-2 infection.</description><identifier>ISSN: 0304-8608</identifier><identifier>EISSN: 1432-8798</identifier><identifier>DOI: 10.1007/s00705-021-05247-z</identifier><identifier>PMID: 34554303</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Asymptomatic ; Biomarkers ; Biomarkers - blood ; Biomedical and Life Sciences ; Biomedicine ; Chemokine CXCL10 ; Chemokines ; Chemokines - immunology ; Coronaviruses ; COVID-19 ; COVID-19 - diagnosis ; COVID-19 - immunology ; CXCL10 protein ; Cytokines ; Cytokines - immunology ; Humans ; IL-1β ; Immune system ; India - epidemiology ; Infections ; Infectious Diseases ; Inflammation ; Interleukin 12 ; Interleukin 17 ; Interleukin 4 ; Interleukin 6 ; Interleukin-1beta ; Medical Microbiology ; Morbidity ; Original ; Original Article ; Pandemics ; Patients ; Severe acute respiratory syndrome coronavirus 2 ; Tumor Necrosis Factor-alpha ; Tumor necrosis factor-α ; Vascular endothelial growth factor ; Viral infections ; Virology ; γ-Interferon</subject><ispartof>Archives of virology, 2021-12, Vol.166 (12), p.3301-3310</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-7217cf39921be38edec27763c352492e8859a1012f21e165b496e01d5c9e632e3</citedby><cites>FETCH-LOGICAL-c474t-7217cf39921be38edec27763c352492e8859a1012f21e165b496e01d5c9e632e3</cites><orcidid>0000-0002-8919-3819</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00705-021-05247-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00705-021-05247-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34554303$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tripathy, Anuradha S.</creatorcontrib><creatorcontrib>Vishwakarma, Siddhesh</creatorcontrib><creatorcontrib>Trimbake, Diptee</creatorcontrib><creatorcontrib>Gurav, Yogesh K.</creatorcontrib><creatorcontrib>Potdar, Varsha A.</creatorcontrib><creatorcontrib>Mokashi, Nitin D.</creatorcontrib><creatorcontrib>Patsute, Sudhir D.</creatorcontrib><creatorcontrib>Kaushal, Himanshu</creatorcontrib><creatorcontrib>Choudhary, Manohar L.</creatorcontrib><creatorcontrib>Tilekar, Bipin N.</creatorcontrib><creatorcontrib>Sarje, Prakash</creatorcontrib><creatorcontrib>Dange, Varsha S.</creatorcontrib><creatorcontrib>Abraham, Priya</creatorcontrib><title>Pro-inflammatory CXCL-10, TNF-α, IL-1β, and IL-6: biomarkers of SARS-CoV-2 infection</title><title>Archives of virology</title><addtitle>Arch Virol</addtitle><addtitle>Arch Virol</addtitle><description>Currently, the world is witnessing the pandemic of COVID-19, a disease caused by the novel coronavirus SARS-CoV-2. Reported differences in clinical manifestations and outcomes in SARS-CoV-2 infection could be attributed to factors such as virus replication, infiltration of inflammatory cells, and altered cytokine production. Virus-induced aberrant and excessive cytokine production has been linked to the morbidity and mortality of several viral infections. Using a Luminex platform, we investigated plasma cytokine and chemokine levels of 27 analytes from hospitalized asymptomatic (
n
= 39) and mildly symptomatic (
n
= 35) SARS-CoV-2-infected patients (in the early phase of infection), recovered individuals (45-60 days postinfection) (
n
= 40), and uninfected controls (
n
= 36) from the city of Pune located in the state of Maharashtra in India. Levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α and the chemokine CXCL-10 were significantly higher, while those of the antiviral cytokines IFN-γ and IL-12 p70 were significantly lower in both asymptomatic and mildly symptomatic patients than in controls. Comparison among the patient categories revealed no difference in the levels of the cytokines/chemokines except for CXCL-10 being significantly higher and IL-17, IL-4, and VEGF being significantly lower in the mildly symptomatic patients. Interestingly, levels of all key analytes were significantly lower in recovered individuals than in those in both patient categories. Nevertheless, the level of CXCL10 was significantly higher in the recovered patients than in the controls, indicating that the immune system of SARS-CoV-2 patients may take a longer time to normalize. Our data suggest that IL-6, IL-1β, TNF-α, CXCL-10, and reduced antiviral cytokines could be used as biomarkers of SARS-CoV-2 infection.</description><subject>Asymptomatic</subject><subject>Biomarkers</subject><subject>Biomarkers - blood</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Chemokine CXCL10</subject><subject>Chemokines</subject><subject>Chemokines - immunology</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>COVID-19 - diagnosis</subject><subject>COVID-19 - immunology</subject><subject>CXCL10 protein</subject><subject>Cytokines</subject><subject>Cytokines - immunology</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immune system</subject><subject>India - epidemiology</subject><subject>Infections</subject><subject>Infectious Diseases</subject><subject>Inflammation</subject><subject>Interleukin 12</subject><subject>Interleukin 17</subject><subject>Interleukin 4</subject><subject>Interleukin 6</subject><subject>Interleukin-1beta</subject><subject>Medical Microbiology</subject><subject>Morbidity</subject><subject>Original</subject><subject>Original Article</subject><subject>Pandemics</subject><subject>Patients</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Tumor Necrosis Factor-alpha</subject><subject>Tumor necrosis factor-α</subject><subject>Vascular endothelial growth factor</subject><subject>Viral infections</subject><subject>Virology</subject><subject>γ-Interferon</subject><issn>0304-8608</issn><issn>1432-8798</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtOHDEQhq0IFAbIBbJALbFhMU78bNtZREItXtIoQYGg7CyPpxqadLeJ3YPE3AoOMmeKYQh5LLKxq1xf_a7Sj9BbSt5RQtT7lA8iMWEUE8mEwotXaEQFZ1gro9fQiHAisC6J3kCbKV0Tkh-4fI02uJBS5HiELk5jwE1ft67r3BDiXVF9qyaYknFx_ukQL-_HxUlOlw_jwvWzx7j8UEyb0Ln4HWIqQl2c7X85w1W4wKzIQuCHJvTbaL12bYI3z_cW-np4cF4d48nno5Nqf4K9UGLAilHla24Mo1PgGmbgmVIl9zzvYxhoLY2jhLKaUaClnApTAqEz6Q2UnAHfQh9XujfzaQczD_0QXWtvYpMHvLPBNfbvSt9c2ctwa7WQhgqZBfaeBWL4MYc02K5JHtrW9RDmyTKppOalEiqju_-g12Ee-7yeZSVhnClOTabYivIxpBShfhmGEvtom13ZZrNt9sk2u8hNO3-u8dLyy6cM8BWQcqm_hPj77__I_gR9UqAj</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Tripathy, Anuradha S.</creator><creator>Vishwakarma, Siddhesh</creator><creator>Trimbake, Diptee</creator><creator>Gurav, Yogesh K.</creator><creator>Potdar, Varsha A.</creator><creator>Mokashi, Nitin D.</creator><creator>Patsute, Sudhir D.</creator><creator>Kaushal, Himanshu</creator><creator>Choudhary, Manohar L.</creator><creator>Tilekar, Bipin N.</creator><creator>Sarje, Prakash</creator><creator>Dange, Varsha S.</creator><creator>Abraham, Priya</creator><general>Springer Vienna</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8919-3819</orcidid></search><sort><creationdate>20211201</creationdate><title>Pro-inflammatory CXCL-10, TNF-α, IL-1β, and IL-6: biomarkers of SARS-CoV-2 infection</title><author>Tripathy, Anuradha S. ; Vishwakarma, Siddhesh ; Trimbake, Diptee ; Gurav, Yogesh K. ; Potdar, Varsha A. ; Mokashi, Nitin D. ; Patsute, Sudhir D. ; Kaushal, Himanshu ; Choudhary, Manohar L. ; Tilekar, Bipin N. ; Sarje, Prakash ; Dange, Varsha S. ; Abraham, Priya</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-7217cf39921be38edec27763c352492e8859a1012f21e165b496e01d5c9e632e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Asymptomatic</topic><topic>Biomarkers</topic><topic>Biomarkers - blood</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Chemokine CXCL10</topic><topic>Chemokines</topic><topic>Chemokines - immunology</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>COVID-19 - diagnosis</topic><topic>COVID-19 - immunology</topic><topic>CXCL10 protein</topic><topic>Cytokines</topic><topic>Cytokines - immunology</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Immune system</topic><topic>India - epidemiology</topic><topic>Infections</topic><topic>Infectious Diseases</topic><topic>Inflammation</topic><topic>Interleukin 12</topic><topic>Interleukin 17</topic><topic>Interleukin 4</topic><topic>Interleukin 6</topic><topic>Interleukin-1beta</topic><topic>Medical Microbiology</topic><topic>Morbidity</topic><topic>Original</topic><topic>Original Article</topic><topic>Pandemics</topic><topic>Patients</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Tumor Necrosis Factor-alpha</topic><topic>Tumor necrosis factor-α</topic><topic>Vascular endothelial growth factor</topic><topic>Viral infections</topic><topic>Virology</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tripathy, Anuradha S.</creatorcontrib><creatorcontrib>Vishwakarma, Siddhesh</creatorcontrib><creatorcontrib>Trimbake, Diptee</creatorcontrib><creatorcontrib>Gurav, Yogesh K.</creatorcontrib><creatorcontrib>Potdar, Varsha A.</creatorcontrib><creatorcontrib>Mokashi, Nitin D.</creatorcontrib><creatorcontrib>Patsute, Sudhir D.</creatorcontrib><creatorcontrib>Kaushal, Himanshu</creatorcontrib><creatorcontrib>Choudhary, Manohar L.</creatorcontrib><creatorcontrib>Tilekar, Bipin N.</creatorcontrib><creatorcontrib>Sarje, Prakash</creatorcontrib><creatorcontrib>Dange, Varsha S.</creatorcontrib><creatorcontrib>Abraham, Priya</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Archives of virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tripathy, Anuradha S.</au><au>Vishwakarma, Siddhesh</au><au>Trimbake, Diptee</au><au>Gurav, Yogesh K.</au><au>Potdar, Varsha A.</au><au>Mokashi, Nitin D.</au><au>Patsute, Sudhir D.</au><au>Kaushal, Himanshu</au><au>Choudhary, Manohar L.</au><au>Tilekar, Bipin N.</au><au>Sarje, Prakash</au><au>Dange, Varsha S.</au><au>Abraham, Priya</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pro-inflammatory CXCL-10, TNF-α, IL-1β, and IL-6: biomarkers of SARS-CoV-2 infection</atitle><jtitle>Archives of virology</jtitle><stitle>Arch Virol</stitle><addtitle>Arch Virol</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>166</volume><issue>12</issue><spage>3301</spage><epage>3310</epage><pages>3301-3310</pages><issn>0304-8608</issn><eissn>1432-8798</eissn><abstract>Currently, the world is witnessing the pandemic of COVID-19, a disease caused by the novel coronavirus SARS-CoV-2. Reported differences in clinical manifestations and outcomes in SARS-CoV-2 infection could be attributed to factors such as virus replication, infiltration of inflammatory cells, and altered cytokine production. Virus-induced aberrant and excessive cytokine production has been linked to the morbidity and mortality of several viral infections. Using a Luminex platform, we investigated plasma cytokine and chemokine levels of 27 analytes from hospitalized asymptomatic (
n
= 39) and mildly symptomatic (
n
= 35) SARS-CoV-2-infected patients (in the early phase of infection), recovered individuals (45-60 days postinfection) (
n
= 40), and uninfected controls (
n
= 36) from the city of Pune located in the state of Maharashtra in India. Levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α and the chemokine CXCL-10 were significantly higher, while those of the antiviral cytokines IFN-γ and IL-12 p70 were significantly lower in both asymptomatic and mildly symptomatic patients than in controls. Comparison among the patient categories revealed no difference in the levels of the cytokines/chemokines except for CXCL-10 being significantly higher and IL-17, IL-4, and VEGF being significantly lower in the mildly symptomatic patients. Interestingly, levels of all key analytes were significantly lower in recovered individuals than in those in both patient categories. Nevertheless, the level of CXCL10 was significantly higher in the recovered patients than in the controls, indicating that the immune system of SARS-CoV-2 patients may take a longer time to normalize. Our data suggest that IL-6, IL-1β, TNF-α, CXCL-10, and reduced antiviral cytokines could be used as biomarkers of SARS-CoV-2 infection.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>34554303</pmid><doi>10.1007/s00705-021-05247-z</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-8919-3819</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Asymptomatic Biomarkers Biomarkers - blood Biomedical and Life Sciences Biomedicine Chemokine CXCL10 Chemokines Chemokines - immunology Coronaviruses COVID-19 COVID-19 - diagnosis COVID-19 - immunology CXCL10 protein Cytokines Cytokines - immunology Humans IL-1β Immune system India - epidemiology Infections Infectious Diseases Inflammation Interleukin 12 Interleukin 17 Interleukin 4 Interleukin 6 Interleukin-1beta Medical Microbiology Morbidity Original Original Article Pandemics Patients Severe acute respiratory syndrome coronavirus 2 Tumor Necrosis Factor-alpha Tumor necrosis factor-α Vascular endothelial growth factor Viral infections Virology γ-Interferon |
| title | Pro-inflammatory CXCL-10, TNF-α, IL-1β, and IL-6: biomarkers of SARS-CoV-2 infection |
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