Publications by authors named "Kaveh Sadeghi"

11 Publications

  • Page 1 of 1

First Cases of SARS-CoV-2 in Iran, 2020: Case Series Report.

Iran J Public Health 2020 Aug;49(8):1564-1568

Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

In Jan 2020, the outbreak of the 2019 novel coronavirus (SARS-CoV-2) in Wuhan, Hubei Province of China spread increasingly to other countries worldwide which WHO declared it as a public health emergency of international concern. Iran was included in the affected countries. Throat swab specimens were collected and tested by using real-time reverse transcription PCR (RT-PCR) kit targeting the E region for screening and RNA dependent RNA polymerase for confirmation. Conventional RT-PCR was conducted for the N region and the PCR products were sequenced by Sanger sequencing. The first seven cases of SARS-CoV-2 infections were identified in Qom, Iran. This report describes the clinical and epidemiological features of the first cases of SARS-CoV-2 confirmed in Iran. Future research should focus on finding the routes of transmission for this virus, including the possibility of transmission from foreign tourists to identify the possible origin of SARS-CoV-2 outbreak in Iran.
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http://dx.doi.org/10.18502/ijph.v49i8.3903DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554384PMC
August 2020

Survey of WU and KI polyomaviruses, coronaviruses, respiratory syncytial virus and parechovirus in children under 5 years of age in Tehran, Iran.

Iran J Microbiol 2020 Apr;12(2):164-169

Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Background And Objectives: Severe acute respiratory infections (SARI) remain an important cause for childhood morbidity worldwide. We designed a research with the objective of finding the frequency of respiratory viruses, particularly WU and KI polyomaviruses (WUPyV & KIPyV), human coronaviruses (HCoVs), human respiratory syncytial virus (HRSV) and human parechovirus (HPeV) in hospitalized children who were influenza negative.

Materials And Methods: Throat swabs were collected from children younger than 5 years who have been hospitalized for SARI and screened for WUPyV, KIPyV, HCoVs, HRSV and HPeV using Real time PCR.

Results: A viral pathogen was identified in 23 (11.16%) of 206 hospitalized children with SARI. The rate of virus detection was considerably greater in infants <12 months (78.2%) than in older children (21.8%). The most frequently detected viruses were HCoVs with 7.76% of positive cases followed by KIPyV (2%) and WUPyV (1.5%). No HPeV and HRSV were detected in this study.

Conclusion: This research shown respiratory viruses as causes of childhood acute respiratory infections, while as most of mentioned viruses usually causes mild respiratory diseases, their frequency might be higher in outpatient children. Meanwhile as HRSV is really sensitive to inactivation due to environmental situations and its genome maybe degraded, then for future studies, we need to use fresh samples for HRSV detection. These findings addressed a need for more studies on viral respiratory tract infections to help public health.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7244825PMC
April 2020

Potential of H1N1 influenza A virus as an air borne pathogen to induce infectivity in pancreas: a mouse model study.

J Environ Health Sci Eng 2020 Jun 17;18(1):303-310. Epub 2020 Mar 17.

1Virology Department, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Introduction: H1N1 influenza virus, as an indoor/outdoor pathogen in air, can cause the flu-like illness and respiratory complication. The aim of this study was to evaluate the H1N1 influenza virus replication in pancreas and investigate the immune response against infected pancreas.

Material And Methods: First, mouse pancreas cell line was infected by H1N1 influenza A virus using intranasally and intravenously infection methods, and then the pancreas tissue was collected and pathology experiment was carried out. Next, the protein and genome of influenza virus were detected using immunocytochemistry and real-time PCR, respectively. In addition, serum cytokines and serum lipase were investigated using ELISA.

Result: The in-vitro results proved that the mouse pancreatic cell line can support influenza virus replication. The result also proved that influenza virus is capable to infect pancreas and induce pancreas damage. Further, the immune response in mice with infected pancreas exhibited a completely different pattern with that of mice infected through intranasal method.

Conclusion: It can be concluded that influenza virus can infect pancreas and change the influenza disease pathway, which might result in a pancreatic injury.
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http://dx.doi.org/10.1007/s40201-020-00468-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7203352PMC
June 2020

A field indoor air measurement of SARS-CoV-2 in the patient rooms of the largest hospital in Iran.

Sci Total Environ 2020 Jul 6;725:138401. Epub 2020 Apr 6.

Department of Virology, School of Public Health, Tehran University of Medical Sciences. Electronic address:

The coronavirus disease 2019 (COVID-19) emerged in Wuhan city, China, in late 2019 and has rapidly spread throughout the world. The major route of transmission of SARS-CoV-2 is in contention, with the airborne route a likely transmission pathway for carrying the virus within indoor environments. Until now, there has been no evidence for detection of airborne severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and this may have implication for the potential spread of the COVID-19. We investigated the air of patient rooms with confirmed COVID-19 in the largest hospital in Iran, on March 17, 2020. To collect the SARS-CoV-2 particles, ten air samples were collected into the sterile standard midget impingers containing 20 mL DMEM with 100 μg/mL streptomycin, 100 U/mL penicillin and 1% antifoam reagent for 1 h. Besides, indoor particle number concentrations, CO, relative humidity and temperature were recorded throughout the sampling duration. Viral RNA was extracted from samples taken from the impingers and Reverse-Transcription PCR (RT-PCR) was applied to confirm the positivity of collected samples based on the virus genome sequence. Fortunately, in this study all air samples which were collected 2 to 5 m from the patients' beds with confirmed COVID-19 were negative. Despite we indicated that all air samples were negative, however, we suggest further in vivo experiments should be conducted using actual patient cough, sneeze and breath aerosols in order to show the possibility of generation of the airborne size carrier aerosols and the viability fraction of the embedded virus in those carrier aerosols.
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http://dx.doi.org/10.1016/j.scitotenv.2020.138401DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7194859PMC
July 2020

Elevated serum levels of adiponectin and interlukin-28B after IFN/RIB therapy in hepatitis C virus-infected patients.

J Infect Dev Ctries 2019 05 31;13(5):434-444. Epub 2019 May 31.

Department of Virology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Introduction: The interleukin 28B (IL28B) genotype is associated with changes of lipid metabolism in patients infected with hepatitis C virus (HCV). The association of steatosis with serum levels of adiponectin in chronic hepatitis C (CHC) patients has also been documented. This study aimed for the evaluation of serum levels of IL28B and adiponectin as well as the association of IL28B SNPs with different clinicopathological parameters in HCV-infected patients.

Methodology: All 142 HCV-infected patients received peg-interferon plus ribavirin. Detection of rs8099917 and rs12979860 IL-28B genotypes was done with specific primers. Serum IL28 and adiponectin levels were measured using commercial ELISA kits.

Results: Higher levels of both IL28 and adiponectin were found in patients. In Genotype 3a (G3a) -infected patients, IL28 and adiponectin serum levels were significantly higher than those infected with G1a. A correlation was found between increasing levels of AST and ALT in G3a-infected patients and the decrease in IL28 and adiponectin serum levels, respectively, in contrast to G1a-infected patients. Higher levels of both IL28 and adiponectin were associated with both CT allele of rs12979860 and TT allele of rs8099917 in patients in comparison with corresponding alleles in controls.

Conclusions: In contrast to other studies, this study showed higher serum adiponectin levels in HCV-infected patients compared to that in healthy controls. This finding is possibly due to adiponectin resistance caused by down-regulation of adiponectin receptors or tumorigenic effects of adiponectin. Our genotype-based analyses revealed, at least in part, the involvement of the viral factors in the outcome of HCV infection.
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http://dx.doi.org/10.3855/jidc.11190DOI Listing
May 2019

Genotype-related variations in proinflammatory and regulatory cytokine levels in treated and treatment-naive HCV-infected patients.

Med Microbiol Immunol 2018 Feb 17;207(1):65-74. Epub 2017 Nov 17.

Department of Microbiology and Immunology, Jahrom University of Medical Sciences, School of Medicine, Motahari Blvd, Jahrom, Iran.

Hepatitis C virus (HCV) modulates immune-related inflammatory responses to induce milder reactions leading to virus persistence. In this regard, the present study aimed to investigate the link between the HCV genotypes and the proinflammatory and regulatory cytokine levels. Ninety patients with hepatitis C infection (68 treatment-naive and 22 treated patients) and 76 healthy blood donors were studied. The serum levels of IFN-γ, IL-10, IL-17A, and IL-21 were measured by ELISA in the patients and healthy controls. IL-10, IL-17A, and IL-21 levels were significantly higher in HCV patients than in the healthy controls. The same cytokines were also higher in genotype 3a-infected patients compared with genotype 1a-infected patients. Interestingly, in treated patients, lower serum levels of IL-17A and IL-21 were detected in G3a-infected individuals, but not in those infected with G1a. G3a viral load displayed a significant correlation with IL-21 and IL-17A levels. In addition, G1a viral load correlated with IL-10 levels. In G3a-infected patients, a significant association was found between IL-17A serum levels and ALT. We found differences in IL-21 and IL-17A serum levels among HCV-infected patients which were genotype dependent. Since Th17-associated cytokines are associated with the progression of liver disease in HCV patients, IL-17A and IL-21 can be used as important biological markers for evaluating the immunopathogenesis of chronic hepatitis. Our results suggest that HCV G3a along with immune responses such as cytokines in HCV patients should be taken into account when interpreting clinical data and IFN-based therapeutic response.
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http://dx.doi.org/10.1007/s00430-017-0527-9DOI Listing
February 2018

Distribution of IL-28B genotypes in patients with hepatitis C and healthy individuals in Jahrom city.

Gastroenterol Hepatol Bed Bench 2015 ;8(4):278-87

Department of Microbiology, Jahrom University of Medical Sciences, Jahrom, Iran.

Aim: The purpose of this study was to compare the distribution of interleukin (IL)-28B genotypes between Iranian healthy individuals and patients with chronic hepatitis C based on the genotype.

Background: Polymorphisms in the region of IL-28B gene have been identified as the strongest genetic pretreatment predictor of sustained virological response (SVR) in hepatitis C infection.

Patients And Methods: In this study, 147 patients with chronic hepatitis C and 80 healthy individuals were included. The IL-28B rs12979860 and rs8099917 polymorphisms were genotyped by PCR-RFLP method and the frequency of IL-28B polymorphisms with respect to HCV genotypes was also determined.

Results: The frequencies of rs12979860 TT, CC and CT genotypes in the chronic hepatitis C patients and healthy individuals were as follows: 10.8% vs. 11.3%, 38.7% vs. 46.2% and 50.3% vs. 42.5%. Also, the frequencies of rs8099917 TT, GG and GT genotypes in the chronic hepatitis C patients was 61.9%, 6.1% and 32% and in controls was 47.5%, 11.2% and 41.3%. The differences in the distribution of rs12979860 genotypes and alleles between HCV genotype 1 and HCV genotype 3a infected patients were statistically significant.

Conclusion: The rs12979860 C allele is the favorable allele for the spontaneous clearance of HCV. It seems that the impact of IL-28B polymorphism on the spontaneous clearance of HCV genotype 3 is more prominent than HCV genotype 1, which results in the observation of higher rs12979860 C allele frequency in chronic hepatitis C patients with HCV genotype 3 than HCV genotype 1.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600518PMC
October 2015

Design of a heterosubtypic epitope-based peptide vaccine fused with hemokinin-1 against influenza viruses.

Virol Sin 2015 Jun 15;30(3):200-7. Epub 2015 Apr 15.

Razi Vaccine & Serum Research Institute, Karaj, 31975, Iran,

Influenza viruses continue to emerge and re-emerge, posing new threats for public health. Control and treatment of influenza depends mainly on vaccination and chemoprophylaxis with approved antiviral drugs. Identification of specific epitopes derived from influenza viruses has significantly advanced the development of epitope-based vaccines. Here, we explore the idea of using HLA binding data to design an epitope-based vaccine that can elicit heterosubtypic T-cell responses against circulating H7N9, H5N1, and H9N2 subtypes. The hemokinin-1 (HK-1) peptide sequence was used to induce immune responses against the influenza viruses. Five conserved high score cytotoxic T lymphocyte (CTL) epitopes restricted to HLA-A*0201-binding peptides within the hemagglutinin (HA) protein of the viruses were chosen, and two HA CTL/HK-1 chimera protein models designed. Using in silico analysis, which involves interferon epitope scanning, protein structure prediction, antigenic epitope determination, and model quality evaluation, chimeric proteins were designed. The applicability of one of these proteins as a heterosubtypic epitopebased vaccine candidate was analyzed.
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http://dx.doi.org/10.1007/s12250-014-3504-0DOI Listing
June 2015

Necrotic Response to Low Pathogenic H9N2 Influenza Virus in Chicken Hepatoma Cells.

Jundishapur J Microbiol 2015 Jan 25;8(1):e13770. Epub 2015 Jan 25.

Social Security Hospital, Khorram Abad, IR Iran.

Background: Limited knowledge about the molecular mechanism of avian influenza H9N2 virus pathogenicity in birds as well as human hosts has limited the development of effective control against the disease. To overcome this issue detailed understanding of the infectious characteristics of the virus in host cells should be obtained.

Objectives: In this study we examined the replication kinetics of H9N2 virus in a chicken hepatoma cell line to obtain insight into the pathogenesis of H9N2 viruses.

Materials And Methods: The kinetic replication of H9N2 influenza virus in chicken hepatoma and fibroblastic cells was studied in the presence and absence of supplemental trypsin. High viral titers observed in liver cells in a short time correlated with the degree of cytopathic effects. To determine whether the ultimate outcome of infection results in programmed cell death, the infected cells were observed by the cell viability assay, DNA fragmentation, caspase cascade activation, and quantified lactate dehydrogenase release.

Results: The degree of viability was significantly reduced in infected hepatoma cells. Observations of caspase activation and cell DNA laddering in infected cells were not indicative of apoptosis. The infected hepatoma cells released lactate dehydrogenase, which is consistent with cell death by necrosis.

Conclusions: Taken together, these data reveal that cellular protease of chicken liver cells allows the replication of high yields of H9N2 virus in the absence of trypsin and also cell death in the infected cells is due to necrosis.
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http://dx.doi.org/10.5812/jjm.13770DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4350051PMC
January 2015

Apoptotic response of chicken embryonic fibroblast cells to infectious bursal disease virus infections reflects viral pathogenicity.

In Vitro Cell Dev Biol Anim 2014 Oct 4;50(9):858-64. Epub 2014 Jul 4.

Razi Vaccine and Serum Research Institute, PO box 31975-148, Karaj, Iran,

Infectious bursal disease virus (IBDV) induces immunodeficiency in young chickens and apoptosis in chicken embryos. To understand the relation between the viral pathogenesis and the induction of cell death, chicken embryonic fibroblast (CEF) cells were infected with IBDV intermediate (im) and very virulent (vv) strains at different MOIs. The cell viability and DNA fragmentation were evaluated in infected cells. The cellular apoptotic pathway involve was investigated by determining the activities of caspase cascade. The imIBDV strain was replicated well in CEF cells and shown higher viral titers than vvIBDV. Apoptosis changes were observed only in vvIBDV-infected CEF cells at higher MOI 48 h post infection. Efflux of cytochrome c suggests that the intrinsic pathway of the apoptotic process induced by vvIBDV infection independently of virus replication. Prediction of caspase substrates cleavage sites revealed that different IBDV strains have conserved cleavage motif pattern for VP2 and VP5 viral proteins. These findings suggest the pathogenicity of IBDV strains might be involved in the induction of apoptosis in host cells.
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http://dx.doi.org/10.1007/s11626-014-9783-9DOI Listing
October 2014

Dose- and time-dependent apoptosis induced by avian H9N2 influenza virus in human cells.

Biomed Res Int 2013 11;2013:524165. Epub 2013 Sep 11.

Razi Vaccine & Serum Research Institute, P.O. Box 31975-148, Karaj 3197619751, Iran.

To understand human response to avian H9N2 influenza, we investigated the effects of the viral infection on A549, HepG2, and HeLa cells at low and high MOIs. To identify virus-host interplay, expression of Mx and NP genes was measured in the cells supernatants. Cell viability and apoptosis were evaluated by MTT assay, DNA fragmentation, and florescent staining. The virus titration and NP gene transcript levels indicate lower susceptibility of HeLa cell to H9N2 replication than other cells. Although H9N2 did produce a faster CPE in HepG2, high dose of the virus induced apoptosis within early stage of A549 infection. The DNA laddering was enhanced in the cell correlated with increase in virus transcripts. The undetectable to different regulation levels of Mx gene were observed in response to H9N2 infection suggesting that an insufficient antiviral defense in the noncompetent-IFN HepG2 cell promotes efficient viral replication. These results showed that the permissivity of HepG2 for H9N2 is comparable with A549; however, liver cells are not target tissue respond to the infection. These data revealed that the H9N2 virus induced apoptosis signaling via mitochondrial pathway in human alveolar epithelial cells, indicating that the induction may be associated with a dose-dependent manner.
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http://dx.doi.org/10.1155/2013/524165DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3784084PMC
June 2014