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Ornek T.,Zonguldak Karaelmas University | YalcIn F.D.,Sanliurfa Education and Research Hospital | Ekin S.,Sanliurfa Education and Research Hospital | YalcIn S.,Harran University | Yemisen M.,Clinic of Infectious Diseases
Wiener Klinische Wochenschrift | Year: 2011

Summary: The objective of this study was to describe the clinical characteristics and the radiological and laboratory findings of the hospitalised patients who had novel, laboratory-confirmed, swine-origin influenza A virus (S-OIV) infection with pneumonia. Between October and December 2009, 56 patients hospitalised for pneumonia who were tested for S-OIV infection were retrospectively evaluated. Thirty-three patients had positive S-OIV infections. In addition, 23 of the 56 patients who had negative test results for S-OIV infection were compared with the positive group. The mortality rate amongst the patients with S-OIV infection was 24.2%. Of the 33 patients, 42.4% had at least one underlying medical condition and 4 (12%) patients were pregnant or postpartum. Fourteen patients (42.4%) with S-OIV infection were followed up in an intensive care unit. The most common symptom was dyspnea. The mean peak body temperature during hospital stay (39.42 ± 0.70) was higher in this group than in the negative group (38.51 ± 1.05) (p = 0.001). Thrombocytopenia, increased creatine kinase and elevated lactate dehydrogenase levels were statistically significant. Bilateral infiltration was more common in the patients with S-OIV infection. Although some laboratory, radiological and clinical data show a significant difference between the patients with S-OIV pneumonia and the negative group, each patient presenting with signs of pneumonia during pandemia should be tested for Influenza A. © 2011 Springer-Verlag.

Fajs L.,University of Ljubljana | Jakupi X.,National Institute of Public Health of Kosovo | Ahmeti S.,Clinic of Infectious Diseases | Humolli I.,National Institute of Public Health of Kosovo | And 2 more authors.
PLoS Neglected Tropical Diseases | Year: 2014

Crimean-Congo hemorrhagic fever virus (CCHFV) is a zoonotic agent that causes severe, life-threatening disease, with a case fatality rate of 10-50%. It is the most widespread tick-borne virus in the world, with cases reported in Africa, Asia and Eastern Europe. CCHFV is a genetically diverse virus. Its genetic diversity is often correlated to its geographical origin. Genetic variability of CCHFV was determined within few endemic areas, however limited data is available for Kosovo. Furthermore, there is little information about the spatiotemporal genetic changes of CCHFV in endemic areas. Kosovo is an important endemic area for CCHFV. Cases were reported each year and the case-fatality rate is significantly higher compared to nearby regions. In this study, we wanted to examine the genetic variability of CCHFV obtained directly from CCHF-confirmed patients, hospitalized in Kosovo from 1991 to 2013. We sequenced partial S segment CCHFV nucleotide sequences from 89 patients. Our results show that several viral variants are present in Kosovo and that the genetic diversity is high in relation to the studied area. We also show that variants are mostly uniformly distributed throughout Kosovo and that limited evolutionary changes have occurred in 22 years. Our results also suggest the presence of a new distinct lineage within the European CCHF phylogenetic clade. Our study provide the largest number of CCHFV nucleotide sequences from patients in 22 year span in one endemic area. © 2014 Fajs et al.

Saksida A.,University of Ljubljana | Duh D.,University of Ljubljana | Wraber B.,University of Ljubljana | Dedushaj I.,University of Prishtina | And 2 more authors.
Clinical and Vaccine Immunology | Year: 2010

Until now, the pathogenesis of Crimean-Congo hemorrhagic fever (CCHF) has not been well described. However, it has been hypothesized that it could be a result of the direct injury of virus-infected tissues in combination with the indirect effects of host immune responses, including cytokines. To shed more light on the role of viral load and cytokines, differential influences of CCHF virus (CCHFV) RNA load, antibody response, and cytokine production on severity and outcome of the disease were studied in sera of 46 patients with confirmed acute CCHF from Kosovo. In this study, viral load proved to be strongly related to the severity and outcome of the disease, with higher viral loads detected in patients with fatal outcomes than in surviving patients. Also, patients with fatal outcome had on average a weaker antibody response, if one was present at all. High levels of interleukin-10 (IL-10), gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α) were associated with poor outcome, since detected concentrations were highest in patients with fatal outcome and lowest in patients with moderate disease course. Additionally, a positive linear dependence between viral load and these cytokines was observed. Interestingly, reduced levels of IL-12 were detected in all CCHF patients. Our study favors the hypothesis that CCHF could be a result of a delayed and downregulated immune response caused by IL-10, which leads to an increased replication and spread of CCHFV throughout the body. This consequently triggers increased production of IFN-γ and TNF-α, cytokines mediating vascular dysfunction, disseminated intravascular coagulation, organ failure, and shock. Copyright © 2010, American Society for Microbiology. All Rights Reserved.

Ghosn J.,Bicetre University Hospital | Carosi G.,University of Brescia | Moreno S.,University of Alcala | Pokrovsky V.,Central Research Institute of Epidemiology | And 7 more authors.
Antiviral Therapy | Year: 2010

Background: Triple combination therapy based on a ritonavir (RTV)-boosted protease inhibitor plus two nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) has improved outcomes in HIV type-1 (HIV-1)-infected patients. For patients unable to tolerate these regimens, alternative therapeutic approaches are needed. Methods: We report a comparative, open-label study in treatment-naive patients who underwent initial induction treatment with a triple combination including RTV-boosted atazanavir (ATV; 300/100 mg once daily). Patients who achieved an HIV-1 viral load <50 copies/ml after the induction period were then randomized in the maintenance phase either to continue on current treatment or to switch to unboosted ATV 400 mg once daily (plus two NRTIs unchanged). Results: A total of 252 patients entered the induction phase, of whom 172 were eligible for randomization in the maintenance phase (ATV/RTV n=85 and ATV n=87). The unboosted ATV regimen demonstrated non-inferior efficacy to the ATV/RTV regimen with 78% and 75% of patients, respectively, maintaining virological suppression (HIV-1 RNA <50 copies/ml) up to week 48 after randomization (difference estimate 2.9, 95% confidence interval -9.8-15.5). Time to virological failure and change from the end of the induction phase in mean CD4+ T-cell counts were also similar between the treatment arms. Although both regimens were well-tolerated, unboosted ATV was associated with fewer adverse events, fewer total bilirubin abnormalities and an improved lipid profile compared with ATV/RTV. Conclusions: An HIV-1 combined treatment regimen based on unboosted ATV is a feasible treatment option for patients with established virological control who are unable to tolerate triple combination therapy including ATV/RTV. ©2010 International Medical Press.

Krut J.J.,Gothenburg University | Krut J.J.,Sahlgrenska University Hospital | Zetterberg H.,Gothenburg University | Blennow K.,Gothenburg University | And 5 more authors.
Journal of Neurology | Year: 2013

The cerebrospinal fluid (CSF) biomarker profile in Alzheimer's disease (AD) is characterized by decreased beta amyloid (Aβ1-42), increased total and hyperphosphorylated tau (t-tau and p-tau, respectively), which is a useful diagnostic tool and gives insight in the pathogenesis of AD. It is of importance to study how these biomarkers react in other CNS diseases; therefore, we decided to analyse amyloid and tau biomarkers in different CNS infections. We also included analysis of soluble amyloid precursor proteins (sAPPα and -β). CSF Aβ1-42, sAPPα and -β, t-tau and p-tau were analysed in bacterial meningitis (n = 12), Lyme neuroborreliosis (n = 13), herpes simplex virus type 1 (HSV-1) encephalitis (n = 10), HIV-associated dementia (HAD) (n = 21), AD (n = 21) and healthy controls (n = 42). Concurrent with AD, Aβ1-42 was decreased in all groups except neuroborreliosis compared to controls. HSV-1 encephalitis, bacterial meningitis and HAD showed lower concentrations of sAPPα and -β compared to AD. T-tau was increased in AD and HSV-1 encephalitis compared to all other groups. P-tau was higher in AD and HSV-1 encephalitis compared to bacterial meningitis, HAD and control. Decreased CSF Aβ1-42, sAPPα and -β in various CNS infections imply an effect of neuroinflammation on amyloid metabolism which is similar in regard to AD concerning Aβ1-42, but differs concerning sAPPα and -β. These results clearly indicate different pathologic pathways in AD and infectious CNS disease and may provide help in the differential biomarker diagnostics. Increased p-tau in HSV-1 encephalitis probably reflect acute neuronal damage and necrosis. © 2012 Springer-Verlag Berlin Heidelberg.

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