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Rasmuson, Johan
Publikasjoner (10 av 12) Visa alla publikasjoner
Gröning, R., Walde, J., Ahlm, C., Forsell, M. N. E., Normark, J. & Rasmuson, J. (2024). Intravenous immunoglobulin therapy for COVID-19 in immunocompromised patients: A retrospective cohort study. International Journal of Infectious Diseases, 144, Article ID 107046.
Åpne denne publikasjonen i ny fane eller vindu >>Intravenous immunoglobulin therapy for COVID-19 in immunocompromised patients: A retrospective cohort study
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2024 (engelsk)Inngår i: International Journal of Infectious Diseases, ISSN 1201-9712, E-ISSN 1878-3511, Vol. 144, artikkel-id 107046Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objectives: To investigate the effectiveness of intravenous immunoglobulin (IVIG) as treatment for COVID-19 in immunocompromised patients.

Methods: This retrospective study investigated outcomes for immunocompromised, vaccine non-responsive, patients that between September 2022 and April 2023 received IVIG as treatment for COVID-19 in the region of Västerbotten, Sweden. We analyzed clinical data, viral load, and anti-SARS-CoV-2 IgG binding and neutralization levels of patient serum samples and IVIG production batches. Primary and secondary outcomes were clinical cure and viral clearance, respectively.

Results: Sixteen patients were analyzed. After a median COVID-19 duration of 4 weeks, a median 60 g IVIG infusion increased SARS-CoV-2 binding and neutralizing antibody levels, with broad in vitro activity against tested variants. The treatment resulted in abrogation of viremia in all patients and general improvement in 15 survivors that all met the primary endpoint. Thirteen patients met the secondary endpoint at follow-up after a median of four months. Two subjects with persistent SARS-CoV-2 carriage relapsed but were successfully retreated with IVIG.

Conclusions: Antibodies in IVIG efficiently neutralized several SARS-CoV-2 variants. Treatment with IVIG was associated with clinical cure and viral clearance in immunocompromised patients. Our data suggests that IVIG could be a novel treatment alternative for COVID-19 for this patient category.

sted, utgiver, år, opplag, sider
Elsevier, 2024
Emneord
COVID-19, Humoral immunity, Immunocompromised, Intravenous immunoglobulin, SARS-CoV-2
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-225264 (URN)10.1016/j.ijid.2024.107046 (DOI)38615825 (PubMedID)2-s2.0-85192717007 (Scopus ID)
Forskningsfinansiär
Umeå UniversityKnut and Alice Wallenberg Foundation, VC-2022-0028Knut and Alice Wallenberg Foundation, VC-2020-0015Knut and Alice Wallenberg Foundation, DNR 2023-01154-01Swedish Research Council, 2020-06235Region Västerbotten, RV-938855Region Västerbotten, RV-939393Swedish Heart Lung Foundation, 20220325
Tilgjengelig fra: 2024-06-10 Laget: 2024-06-10 Sist oppdatert: 2024-06-10bibliografisk kontrollert
Sundén-Cullberg, J., Chen, P., Häbel, H., Skorup, P., Janols, H., Rasmuson, J., . . . Lampa, J. (2023). Anakinra or tocilizumab in patients admitted to hospital with severe covid-19 at high risk of deterioration (IMMCoVA): a randomized, controlled, open-label trial. PLOS ONE, 18(12), Article ID e0295838.
Åpne denne publikasjonen i ny fane eller vindu >>Anakinra or tocilizumab in patients admitted to hospital with severe covid-19 at high risk of deterioration (IMMCoVA): a randomized, controlled, open-label trial
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2023 (engelsk)Inngår i: PLOS ONE, E-ISSN 1932-6203, Vol. 18, nr 12, artikkel-id e0295838Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: Anakinra and tocilizumab are used for severe Covid-19, but only one previous randomized controlled trial (RCT) has studied both. We performed a multi-center RCT comparing anakinra or tocilizumab versus usual care (UC) for adults at high risk of deterioration.

Methods: The study was conducted June 2020 to March 2021. Eligibility required ≥ 5 liters/minute of Oxygen to maintain peripheral oxygen saturation at ≥ 93%, CRP > 70 mg/L, ferritin > 500 μg/L and at least two points where one point was awarded for lymphocytes < 1x 109/L; D-dimer ≥ 0.5 mg/L and; lactate dehydrogenase ≥ 8 microkatal/L. Patients were randomly assigned 1:1:1 to receive either a single dose of tocilizumab (8 mg/kg) or anakinra 100 mg IV QID for seven days or UC alone. The primary outcome was time to recovery.

Results: Recruitment was ended prematurely when tocilizumab became part of usual care. Out of a planned 195 patients, 77 had been randomized, 27 to UC, 28 to anakinra and 22 to tocilizumab. Median time to recovery was 15, 15 and 11 days. Rate ratio for recovery for UC vs anakinra was 0.91, 0.47 to 1.78, 95% [CI], p = 0.8 and for UC vs tocilizumab 1.13, 0.55 to 2.30; p = 0.7. There were non-significant trends favoring tocilizumab (and to limited degree anakinra) vs UC for some secondary outcomes. Safety profiles did not differ significantly.

Conclusion: Premature closure of trial precludes firm conclusions. Anakinra or tocilizumab did not significantly shorten time to clinical recovery compared to usual care. (IMMCoVA, NCT04412291, EudraCT: 2020–00174824).

sted, utgiver, år, opplag, sider
Public Library of Science (PLoS), 2023
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-219336 (URN)10.1371/journal.pone.0295838 (DOI)38157348 (PubMedID)2-s2.0-85181253715 (Scopus ID)
Forskningsfinansiär
Swedish Research Council, 2020-06318
Tilgjengelig fra: 2024-01-11 Laget: 2024-01-11 Sist oppdatert: 2024-01-11bibliografisk kontrollert
Tuiskunen-Bäck, A., Rasmuson, J., Thunberg, T., Rankin, G., Wigren Byström, J., Andersson, C., . . . Ahlm, C. (2022). Clinical and genomic characterisation of a fatal Puumala orthohantavirus case with low levels of neutralising antibodies. Infectious Diseases, 54(10), 766-772
Åpne denne publikasjonen i ny fane eller vindu >>Clinical and genomic characterisation of a fatal Puumala orthohantavirus case with low levels of neutralising antibodies
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2022 (engelsk)Inngår i: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 54, nr 10, s. 766-772Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Orthohantaviruses are rodent-borne emerging viruses that cause haemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus pulmonary syndrome in America. Transmission between humans have been reported and the case-fatality rate ranges from 0.4% to 40% depending on virus strain. There is no specific and efficient treatment for patients with severe HFRS. Here, we characterised a fatal case of HFRS and sequenced the causing Puumala orthohantavirus (PUUV).

METHODS: PUUV RNA and virus specific neutralising antibodies were quantified in plasma samples from the fatal case and other patients with non-fatal PUUV infection. To investigate if the causing PUUV strain was different from previously known strains, Sanger sequencing was performed directly from the patient's plasma. Biopsies obtained from autopsy were stained for immunohistochemistry.

RESULTS: The patient had approximately tenfold lower levels of PUUV neutralising antibodies and twice higher viral load than was normally seen for patients with less severe PUUV infection. We could demonstrate unique mutations in the S and M segments of the virus that could have had an impact on the severity of infection. Due to the severe course of infection, the patient was treated with the bradykinin receptor inhibitor icatibant to reduce bradykinin-mediated vessel permeability and maintain vascular circulation.

CONCLUSIONS: Our data suggest that bradykinin receptor inhibitor may not be highly efficient to treat patients that are at an advanced stage of HFRS. Low neutralising antibodies and high viral load at admission to the hospital were associated with the fatal outcome and may be useful for future predictions of disease outcome.

Emneord
Icatibant, Puumala orthohantavirus, neutralising antibodies, orthohantavirus, viral load, virus sequence
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-201272 (URN)10.1080/23744235.2022.2076904 (DOI)000812658600001 ()35713235 (PubMedID)2-s2.0-85132173959 (Scopus ID)
Forskningsfinansiär
Region Västerbotten, RV-938855Region Västerbotten, RV-734361Swedish Heart Lung Foundation, 2017-0334Swedish Research Council, 2020-06235Lars Hierta Memorial Foundation, FO2018- 0470
Tilgjengelig fra: 2022-11-25 Laget: 2022-11-25 Sist oppdatert: 2022-11-28bibliografisk kontrollert
Connolly-Andersen, A.-M., Rasmuson, J., Öman, M. & Ahlm, C. (2018). Mesenteric Vein Thrombosis Following Platelet Transfusion in a Patient with Hemorrhagic Fever with Renal Syndrome: A Case Report. TH open : companion journal to thrombosis and haemostasis, 2(3), e261-e264
Åpne denne publikasjonen i ny fane eller vindu >>Mesenteric Vein Thrombosis Following Platelet Transfusion in a Patient with Hemorrhagic Fever with Renal Syndrome: A Case Report
2018 (engelsk)Inngår i: TH open : companion journal to thrombosis and haemostasis, ISSN 2567-3459, Vol. 2, nr 3, s. e261-e264Artikkel i tidsskrift (Fagfellevurdert) Published
sted, utgiver, år, opplag, sider
Georg Thieme Verlag KG, 2018
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-183977 (URN)10.1055/s-0038-1669456 (DOI)31249949 (PubMedID)
Tilgjengelig fra: 2021-06-07 Laget: 2021-06-07 Sist oppdatert: 2021-06-07bibliografisk kontrollert
Sironen, T., Sane, J., Lokki, M.-L., Meri, S., Andersson, L. C., Hautala, T., . . . Vaheri, A. (2017). Fatal Puumala Hantavirus Disease: Involvement of Complement Activation and Vascular Leakage in the Pathobiology. Open Forum Infectious Diseases, 4(4), Article ID ofx229.
Åpne denne publikasjonen i ny fane eller vindu >>Fatal Puumala Hantavirus Disease: Involvement of Complement Activation and Vascular Leakage in the Pathobiology
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2017 (engelsk)Inngår i: Open Forum Infectious Diseases, ISSN 2328-8957, Vol. 4, nr 4, artikkel-id ofx229Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The case-fatality rate of hantavirus disease depends strongly on the causative hantavirus, ranging from 0.1% to 40%. However, the pathogenesis is not fully understood, and at present no licensed therapies exist. We describe fatal cases caused by Puumala hantavirus indicating involvement of complement activation and vascular leakage.

sted, utgiver, år, opplag, sider
Oxford University Press, 2017
Emneord
case-fatality rate, complement, hantavirus, Puumala virus, vascular leakage
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-144431 (URN)10.1093/ofid/ofx229 (DOI)000419560500051 ()29255728 (PubMedID)2-s2.0-85072107619 (Scopus ID)
Tilgjengelig fra: 2018-02-02 Laget: 2018-02-02 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Scholz, S., Baharom, F., Rankin, G., Maleki, K. T., Gupta, S., Vangeti, S., . . . Smed-Sörensen, A. (2017). Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways. PLoS Pathogens, 13(6), Article ID e1006462.
Åpne denne publikasjonen i ny fane eller vindu >>Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways
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2017 (engelsk)Inngår i: PLoS Pathogens, ISSN 1553-7366, E-ISSN 1553-7374, Vol. 13, nr 6, artikkel-id e1006462Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Hantaviruses infect humans via inhalation of virus-contaminated rodent excreta. Infection can cause severe disease with up to 40% mortality depending on the viral strain. The virus primarily targets the vascular endothelium without direct cytopathic effects. Instead, exaggerated immune responses may inadvertently contribute to disease development. Mononuclear phagocytes (MNPs), including monocytes and dendritic cells (DCs), orchestrate the adaptive immune responses. Since hantaviruses are transmitted via inhalation, studying immunological events in the airways is of importance to understand the processes leading to immunopathogenesis. Here, we studied 17 patients infected with Puumala virus that causes a mild form of hemorrhagic fever with renal syndrome (HFRS). Bronchial biopsies as well as longitudinal blood draws were obtained from the patients. During the acute stage of disease, a significant influx of MNPs expressing HLA-DR, CD11c or CD123 was detected in the patients' bronchial tissue. In parallel, absolute numbers of MNPs were dramatically reduced in peripheral blood, coinciding with viremia. Expression of CCR7 on the remaining MNPs in blood suggested migration to peripheral and/or lymphoid tissues. Numbers of MNPs in blood subsequently normalized during the convalescent phase of the disease when viral RNA was no longer detectable in plasma. Finally, we exposed blood MNPs in vitro to Puumala virus, and demonstrated an induction of CCR7 expression on MNPs. In conclusion, the present study shows a marked redistribution of blood MNPs to the airways during acute hantavirus disease, a process that may underlie the local immune activation and contribute to immunopathogenesis in hantavirus-infected patients.

sted, utgiver, år, opplag, sider
Public library science, 2017
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-137809 (URN)10.1371/journal.ppat.1006462 (DOI)000404511700047 ()28640917 (PubMedID)2-s2.0-85021833293 (Scopus ID)
Tilgjengelig fra: 2017-07-26 Laget: 2017-07-26 Sist oppdatert: 2024-04-09bibliografisk kontrollert
Rasmuson, J., Pourazar, J., Mohamed, N., Lejon, K., Evander, M., Blomberg, A. & Ahlm, C. (2016). Cytotoxic immune responses in the lungs correlate to disease severity in patients with hantavirus infection. European Journal of Clinical Microbiology and Infectious Diseases, 35(4), 713-721
Åpne denne publikasjonen i ny fane eller vindu >>Cytotoxic immune responses in the lungs correlate to disease severity in patients with hantavirus infection
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2016 (engelsk)Inngår i: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 35, nr 4, s. 713-721Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Hantavirus infections may cause severe and sometime life-threatening lung failure. The pathogenesis is not fully known and there is an urgent need for effective treatment. We aimed to investigate the association between pulmonary viral load and immune responses, and their relation to disease severity. Bronchoscopy with sampling of bronchoalveolar lavage (BAL) fluid was performed in 17 patients with acute Puumala hantavirus infection and 16 healthy volunteers acting as controls. Lymphocyte subsets, granzyme concentrations, and viral load were determined by flow cytometry, enzyme-linked immunosorbent assay (ELISA), and quantitative reverse transcription polymerase chain reaction (RT-PCR), respectively. Analyses of BAL fluid revealed significantly higher numbers of activated CD8+ T cells and natural killer (NK) cells, as well as higher concentrations of the cytotoxins granzymes A and B in hantavirus-infected patients, compared to controls. In patients, Puumala hantavirus RNA was detected in 88 % of BAL cell samples and correlated inversely to the T cell response. The magnitude of the pulmonary cytotoxic lymphocyte response correlated to the severity of disease and systemic organ dysfunction, in terms of need for supplemental oxygen treatment, hypotension, and laboratory data indicating renal failure, cardiac dysfunction, vascular leakage, and cell damage. Regulatory T cell numbers were significantly lower in patients compared to controls, and may reflect inadequate immune regulation during hantavirus infection. Hantavirus infection elicits a pronounced cytotoxic lymphocyte response in the lungs. The magnitude of the immune response was associated with disease severity. These results give insights into the pathogenesis and possibilities for new treatments.

Emneord
hantavirus, hemorrhagic fever with renal syndrome, bronchoalveolar lavage, granzymes, viral load, cytotoxic T-lymphocytes, regulatory T-cells
HSV kategori
Forskningsprogram
infektionssjukdomar
Identifikatorer
urn:nbn:se:umu:diva-99100 (URN)10.1007/s10096-016-2592-1 (DOI)000373300000023 ()26873376 (PubMedID)2-s2.0-84957934487 (Scopus ID)
Merknad

Originally included in thesis in manuscript form

Tilgjengelig fra: 2015-02-04 Laget: 2015-02-04 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Rasmuson, J. (2015). Cardiopulmonary involvement in Puumala hantavirus infection. (Doctoral dissertation). Umeå: Umeå Universitet
Åpne denne publikasjonen i ny fane eller vindu >>Cardiopulmonary involvement in Puumala hantavirus infection
2015 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Puumala hantavirus (PUUV) causes hemorrhagic fever with renal syndrome in Europe. After inhalation of virus shed by bank voles, the virus systemically targets the vascular endothelium leading to vascular dysfunction and leakage. Many patients with PUUV infection experience cardiopulmonary manifestations but the underlying mechanisms have not been determined.

The aims of the studies presented were to describe cardiopulmonary manifestations, investigate pathogenetic mechanisms including presence of virus in the lungs and the local immune response in PUUV infection.

The results showed cardiopulmonary involvement of varying severity in almost all studied patients. High-resolution computed tomography frequently revealed vascular leakage into the lungs or pleural cavities. Pulmonary function tests generally showed reduced gas diffusing capacity, evidenced in patients as dyspnea, poor oxygenation and frequent need of oxygen treatment. Among patients who were not fully recovered at 3 months follow-up, remaining decreased gas diffusing capacity was highly common.

Echocardiography revealed mainly right heart dysfunction which was related to manifestations within the lungs, in terms of increased estimated pulmonary vascular resistance, mild to moderate pulmonary hypertension, and reduced right ventricular systolic function in patients with more pronounced lung involvement, as indicated by need of oxygen treatment.

Analyses on bronchoalveolar lavage (BAL) and bronchial biopsies revealed a highly activated cytotoxic T cell (CTL) response in the lungs. The CTL response was not balanced by the expansion of regulatory T cells and high numbers of CTLs were associated with more severe disease. PUUV RNA was detected in almost all patients’ BAL samples and the viral load was inversely correlated to the number of CTLs.

Three patients presenting with severe and fatal cardiopulmonary distress were also described. Autopsies revealed PUUV protein in vascular endothelium in all investigated organs, including the heart and lungs, along with a massive CTL response mainly in the lungs.

In conclusion, cardiopulmonary involvement of varying severity was present in almost all patients with PUUV infection. Cytotoxic immune responses could contribute to disease development but also help in clearing the infection. Long lasting fatigue after hantavirus infection may be explained by remaining manifestations within the lungs. 

sted, utgiver, år, opplag, sider
Umeå: Umeå Universitet, 2015. s. 69
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1698
Emneord
Hemorrhagic fever with renal syndrome, hantavirus, echocardiography, respiratory function tests, computed tomography, bronchoalveolar lavage, biopsy, cytotoxic T cells, disease severity
HSV kategori
Forskningsprogram
infektionssjukdomar
Identifikatorer
urn:nbn:se:umu:diva-99103 (URN)978-91-7601-215-4 (ISBN)
Disputas
2015-02-27, E04, byggnad 6E, Norrlands Universitetssjukhus, Umeå, 09:00 (engelsk)
Opponent
Veileder
Tilgjengelig fra: 2015-02-06 Laget: 2015-02-04 Sist oppdatert: 2023-05-09bibliografisk kontrollert
Rasmuson, J., Lindqvist, P., Sörensen, K., Hedström, M., Blomberg, A. & Ahlm, C. (2013). Cardiopulmonary involvement in Puumala hantavirus infection. BMC Infectious Diseases, 13(1), 501
Åpne denne publikasjonen i ny fane eller vindu >>Cardiopulmonary involvement in Puumala hantavirus infection
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2013 (engelsk)Inngår i: BMC Infectious Diseases, E-ISSN 1471-2334, Vol. 13, nr 1, s. 501-Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Hantavirus infections cause potentially life-threatening disease in humans world-wide. Infections with American hantaviruses may lead to hantavirus pulmonary syndrome characterised by severe cardiopulmonary distress with high mortality. Pulmonary involvement in European Puumala hantavirus (PUUV) infection has been reported, whereas knowledge of potential cardiac manifestations is limited. We aimed to comprehensively investigate cardiopulmonary involvement in patients with PUUV-infection.

METHODS: Twenty-seven hospitalised patients with PUUV-infection were examined with lung function tests, chest high-resolution CT (HRCT), echocardiography including speckle tracking strain rate analysis, ECG and measurements of cardiac biomarkers N-terminal pro-B-type natriuretic peptide (NT-ProBNP) and troponin T. Patients were re-evaluated after 3 months. Twenty-five age and sex-matched volunteers acted as controls for echocardiography data.

RESULTS: Two-thirds of the patients experienced respiratory symptoms as dry cough or dyspnoea. Gas diffusing capacity was impaired in most patients, significantly improving at follow-up but still subnormal in 38%. HRCT showed thoracic effusions or pulmonary oedema in 46% of the patients. Compared to controls, the main echocardiographic findings in patients during the acute phase were significantly higher pulmonary vascular resistance, higher systolic pulmonary artery pressure, lower left ventricular ejection fraction and impaired left atrial myocardial motion. Pathological ECG, atrial fibrillation or T-wave changes, was demonstrated in 26% of patients. NT-ProBNP concentrations were markedly increased and were inversely associated with gas diffusing capacity but positively correlated to pulmonary vascular resistance. Furthermore, patients experiencing impaired general condition at follow-up had significantly lower gas diffusing capacity and higher pulmonary vascular resistance, compared to those feeling fully recovered.

CONCLUSIONS: In a majority of patients with PUUV-infection, both cardiac and pulmonary involvement was demonstrated with implications on patients' recovery. The results demonstrate vascular leakage in the lungs that most likely is responsible for impaired gas diffusing capacity and increased pulmonary vascular resistance with secondary pulmonary hypertension and right heart distress. Interestingly, NT-ProBNP was markedly elevated even in the absence of overt ventricular heart failure. The method of simultaneous investigations of important cardiac and respiratory measurements improves the interpretation of the underlying pathophysiologic mechanisms.

sted, utgiver, år, opplag, sider
BioMed Central, 2013
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-83698 (URN)10.1186/1471-2334-13-501 (DOI)000328902800001 ()24160911 (PubMedID)2-s2.0-84886124590 (Scopus ID)
Tilgjengelig fra: 2013-12-04 Laget: 2013-12-04 Sist oppdatert: 2024-01-17bibliografisk kontrollert
Pettersson, L., Rasmuson, J., Andersson, C., Ahlm, C. & Evander, M. (2011). Hantavirus-specific IgA in saliva and viral antigen in the parotid gland in patients with hemorrhagic fever with renal syndrome. Journal of Medical Virology, 83(5), 864-870
Åpne denne publikasjonen i ny fane eller vindu >>Hantavirus-specific IgA in saliva and viral antigen in the parotid gland in patients with hemorrhagic fever with renal syndrome
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2011 (engelsk)Inngår i: Journal of Medical Virology, ISSN 0146-6615, E-ISSN 1096-9071, Vol. 83, nr 5, s. 864-870Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The Hantavirus genus comprises rodent borne, zoonotic viruses of the Bunyaviridae family that cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Rodent saliva contains infectious hantavirus and evidence suggests that hantavirus is also shed in human saliva, but person-to-person transmission is rare. In saliva, immunoglobulin (Ig) A is the predominant immunoglobulin class. Secretory IgA serves as an important first line of defence on epithelial surfaces and the binding of secretory IgA to pathogens can inhibit adherence of microorganisms to mucosal cells and neutralize viruses. This study investigated the presence and importance of salivary IgA in relation to viral antigen in the saliva by testing Puumala hantavirus (PUUV) specific IgA, and RNA in saliva in acutely ill patients with HFRS. In saliva samples, PUUV specific IgA was detected in 12 of 33 (36%) patients with HFRS and 20 (61%) were PUUV RNA positive. There was a statistically significant inverse association between the presence of salivary IgA antibodies and PUUV RNA in the saliva. PUUV-specific IgA in saliva was not found in a long-term follow-up, while PUUV IgA in serum was detected in three patients, 28-32 months after the initial study. Notably, both PUUV RNA and PUUV nucleocapsid antigen were detected in endothelial cells within the parotid gland of a deceased patient with HFRS. J. Med. Virol. 83:864-870, 2011. © 2011 Wiley-Liss, Inc.

Emneord
puumalavirus;HFRS;HCPS;antibody;zoonosis;transmission
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-41725 (URN)10.1002/jmv.22040 (DOI)21360546 (PubMedID)2-s2.0-79952721391 (Scopus ID)
Tilgjengelig fra: 2011-03-31 Laget: 2011-03-31 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Organisasjoner