In vitro detection of hepatitis C virus in platelets from uninfected individuals exposed to the virus

Padovani, Juliana Lara; Corvino, Sílvia Maria; Drexler, Jan Felix; Silva, Giovanni Faria; Pardini, Maria Inês de Moura Campos; Grotto, Rejane Maria Tommasini

doi:10.1590/0037-8682-1627-2013

Cited by 11 publications

(18 citation statements)

References 12 publications

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“…The main receptor for HCV in hepatocytes is cluster differentiation 81 (CD81) molecule, which is not expressed on platelets. Recently, a study showed that HCV interacts with platelets despite the absence of the receptor CD81 molecule (Padovani et al, 2013). Pugliese et al (2004) However, the role of HPA-2 in the interaction of HCV with platelets remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Association of human platelet antigens polymorphisms with susceptibility to hepatitis C virus infection in Chinese population

Zhou¹,

Liang²,

Shao³

et al. 2017

Int J Immunogenetics

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Hepatitis C virus (HCV) is a major cause of chronic hepatitis. Previous studies have identified a number of single nucleotide polymorphisms that are associated with HCV infection. Human platelet antigens (HPAs) polymorphisms play an important role in several diseases. Here, we demonstrated the association of the HPA-2, HPA-3, HPA-5 and HPA-15 polymorphisms with susceptibility to HCV infection in Chinese population. Overall, 118 patients with HCV and 167 controls were genotyped for HPAs. There were no significant differences in the allele and genotype frequency distribution for the HPA-3, HPA-5 and HPA-15 systems between the patients with chronic HCV infection and the healthy controls (p > .05). However, the genotype frequency of HPA-2aa was significantly lower, while HPA-2ab/bb was significantly higher in patients than that in the controls (p = .006). The allele frequency of HPA-2a in patients was significantly lower than that in the control group (p = .005). In contrast, HPA-2b in patients was significantly higher than that in the control group (p = .005). We conclude that HPA-2 polymorphism is associated with susceptibility to HCV infection, and individuals carrying the HPA-2b allele may have a higher risk of HCV infection compared with individuals carrying HPA-2a.

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Section: Discussionmentioning

confidence: 99%

Association of human platelet antigens polymorphisms with susceptibility to hepatitis C virus infection in Chinese population

Zhou¹,

Liang²,

Shao³

et al. 2017

Int J Immunogenetics

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“…We also found that, those who relapsed had detectable HCV-RNA in their platelets in spite of being negative in peripheral blood. Platelets do not express CD81 or the classical LDL-R, suggesting that other receptors/ molecules are involved in the entry of HCV-RNA to the platelets [16]. HCV interaction with the platelet membrane glycoprotein VI, might explain the viral binding to platelets in infected patients [17].…”

Section: Discussionmentioning

confidence: 99%

Platelets as a Possible Reservoir of HCV And Predictor of Response to Treatment

Amer¹,

Madi²,

Shebl³

et al. 2016

J Virol Antivir Res

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In the era of new Hepatitis C Virus (HCV) therapy, and the detection of extrahepatic HCV reservoirs such as peripheral blood mononuclear cells and platelets, it is important to understand the factors underlying resistance to treatment. Detection and quantitation of HCV-RNA in platelets or leucocytes from patients under antiviral therapy is poorly studied and the limited studies generated contradictory results. Aim:To detect and quantify HCV-RNA in platelets, and to evaluate the relation between HCV-RNA in the serum and the kinetics of HCV-RNA in platelets, in response to treatment.Method: Viral kinetic was tested in 20 chronic HCV genotype4, during the course of therapy.Results: HCV-RNA was detected in sera of all infected patients. The baseline platelet viral load was significantly lower in responders compared to non-responders. Platelet viral load was also related to serum viral load (t=3.39, p=0.001), but not related to platelet count (t=-0.56, p=0.58). ROC curve analysis revealed that in general, platelet viral load at different time points was a better predictor of SVR compared to serum viral load.Conclusion: HCV RNA analysis in whole blood may be more sensitive than platelet-poor plasma, which might underestimate circulating viral load. Early eradication of viremia from platelets is associated with higher rates of SVR. Our data, reconfirm higher HCV-RNA levels in serum compared to platelets. Thrombocytopenia occurring during interferon-based therapy might be a manifestation of viral eradication rather than adverse effects. Our findings warrant testing the sensitivity of platelet viral load as a predictor of poor response.

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“…Ribonucleic acid from platelets was obtained according to Padovani et al 13 . RNA extracted from hepatic tissue and platelets was used as a source to perform reverse-strand complementary deoxyribonucleic acid (cDNA) synthesis using the HighCapacity cDNA Archive kit (Thermo Fisher Scientific, Inc., CA, USA), according to the manufacturer's specifications.…”

Section: Tablementioning

confidence: 99%

Platelet-derived growth factor A mRNA in platelets is associated with the degree of hepatic fibrosis in chronic hepatitis C

Tanikawa

Grotto

Silva

et al. 2017

Rev. Soc. Bras. Med. Trop.

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Abstract:Introduction: Transforming growth factor beta 1 (TGFB1) and platelet-derived growth factor (PDGF) are the main cytokines related to hepatic fibrogenesis. Methods: RNA isolated from the platelets and hepatic tissue of 43 HCV carriers was used for quantitative polymerase chain reaction to determine TGFB1, PDGFA, and PDGFB RNA expression. Results: The mRNA expression of PDGFA in platelets was significantly lower in the group with advanced fibrosis than in the group with earlystage fibrosis. TGFB1 was more frequently expressed in platelets than in hepatic tissue, which was different from PDGFB. Conclusions: A pathway mediated by overexpression of TGFB1 via PDGFA in megakaryocytes could be involved in the development of fibrosis.Keywords: Hepatic fibrosis. PDGF. TGFB.Hepatic fibrosis, a consequence of various chronic stimuli, including infection with hepatitis C virus (HCV), is characterized by the progressive accumulation of extracellular matrix (ECM) components in the hepatic parenchyma, which leads to a progressive replacement of the functional tissue with scar tissue 1 .Hepatic stellate cells (HSCs) are considered the main cells producing ECM proteins 2 and their activation and proliferation are mediated by two cytokines, transforming growth factor beta 1 (TGFB1) and platelet-derived growth factor (PDGF). Both are secreted by HSCs, platelets, and other cells 3,4 .Transforming growth factor beta 1 is the major profibrogenic cytokine in the liver because of its contribution to fibrosis development via HSC activation and the regulation of gene expression associated with signaling cascades related to fibrosis 5,6 . Platelet-derived growth factor is the most potent mitogen for HSCs 7 . There are four different PDGF isoforms 8 and the PDGFB isoform is considered the most important mitogen for HSCs [7][8][9] . However, studies have demonstrated that PDGFA can also be considered an important profibrogenic agent, acting via TGFB1 induction 10 .Considering that platelets are major sources of TGFB1 and PDGF, which are growth factors involved in the development of liver fibrosis associated with chronic hepatitis C, and that studies have already demonstrated that platelets that accumulate in the liver during chronic hepatitis may be involved in hepatic fibrosis 11 , the aim of this study was to evaluate the expressions of PDGFA, PDGFB, and TGFB1 in hepatic tissue and platelets from HCV-infected patients presenting with varying degrees of hepatic fibrosis.Aliquots of ethylenediaminetetraacetic acid (EDTA)-anticoagulated peripheral venous blood and fragments of hepatic tissue were collected from 43 HCV-infected patients who presented at the Department of Internal Medicine, Gastroenterology Division, Botucatu Medical School, São Paulo State University [Universidade Estadual Paulista (UNESP)], Botucatu, SP, Brazil. The inclusion criteria were naïve patients infected with HCV genotype 1 who were aged >18 years, had undergone a liver biopsy before the start of antiviral treatment, and had signed informed consent. The exclu...

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In vitro detection of hepatitis C virus in platelets from uninfected individuals exposed to the virus

Cited by 11 publications

References 12 publications

Association of human platelet antigens polymorphisms with susceptibility to hepatitis C virus infection in Chinese population

Association of human platelet antigens polymorphisms with susceptibility to hepatitis C virus infection in Chinese population

Platelets as a Possible Reservoir of HCV And Predictor of Response to Treatment

Platelet-derived growth factor A mRNA in platelets is associated with the degree of hepatic fibrosis in chronic hepatitis C

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