Reciprocal Changes of Naïve and Effector/Memory CD8<sup>+</sup> T Lymphocytes in Chronic Hepatitis B Virus Infection

Carotenuto, P; Artsen, Andrè; Osterhaus, Albert D. M. E.; Pontesilli, O.

doi:10.1089/vim.2010.0067

Cited by 5 publications

(4 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These viruses affect the immune system by increasing immune activation and causing changes to T cell subset distribution (7,8,12,14,27). Our previous research (14) and that of others (5,7,9,11,27) have shown the importance of CD4…”

mentioning

confidence: 90%

See 1 more Smart Citation

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

et al. 2016

View full text Add to dashboard Cite

Intravenous drug use (IDU) is one of the most important transmission routes for blood borne viruses, including human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These infections alter the subset distributions of T cells; however, knowledge of such effects during HIV, HBV, and or HCV coinfection is limited. Therefore, we aimed to evaluate any associations between T cell distribution and the presence of HIV, HBV, and HCV coinfections among persons who inject drugs (PWID). Blood samples from 88 Caucasian PWID (mean age 30; 82% male) and 47 age-matched subjects negative for all three infections (mean age of 29; 83% male) were analyzed. The T cell markers CD3, CD4, CD8, CD45RA, CCR7, HLA-DR, and CCR5 were assessed using flow cytometry. Of the PWID, 40% were HIV+HBV+HCV+, 20% HBV+HCV+, 19% HCV+, and 13% negative for all three infections. The HIV+HBV+HCV+ PWID had lower percentages of CD4 + and higher percentages of CD8 + cells compared to triple negative PWID ( p < 0.001 in all cases). The only difference between HBV+HCV+ with triple negative PWID was the lower CD4 + cell percentages among the former (52.1% and 58.6%, p = 0.021). Triple negative PWID had higher immune activation and number of CCR5+ cells compared to the controls. We suggest that the altered T cell subset distribution among PWID is mainly triggered by HIV infection and or IDU, while HBV and or HCV seropositivity has minimal additional effects on CD4 + cell distribution.

show abstract

mentioning

confidence: 90%

“…+ T CM and T EM CD8 + cell populations through the acute to chronic phase of the illness has mainly been noted (1,5,28). In addition, an overall decrease in the number of CD4 + T cells has been found among HBV and HCV mono-infected chimpanzees, together with inadequate CD8…”

Section: Figmentioning

confidence: 99%

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The impact of innate immunity in liver damage also has been identified in several studies [10, 11]. Toll-like receptors (TLRs) describe a group of pattern recognition receptors (PRRs) playing critical roles in the host innate immune response [12].…”

Section: Introductionmentioning

confidence: 99%

The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation

Moradzadeh

Tayebi

Sayehmiri

et al. 2013

Advances in Virology

View full text Add to dashboard Cite

Recognition mechanisms of innate immune response help to improve immunotherapeutic strategies in HBeAg-negative chronic hepatitis B (CHB). Toll-like receptor 2 (TLR2) is an important component of innate immunity. In this study, the frequency of precore mutations of the hepatitis B virus (HBV) and serum TLR2 were evaluated in CHB patients. Fifty-one patients with chronic hepatitis B, negative for HBeAg and detectable HBV DNA, were examined for the presence of mutations in pre-core region of HBV genome by direct sequencing. Serum TLR2 was measured by enzyme-linked immunosorbent assay. Interactions of truncated HBeAg and TLR2 proteins were evaluated with molecular docking software. The G1896A pre-core mutation were detected in 29 (57%) which was significantly associated with higher concentration of serum TLR2 in comparison with patients without this mutation (4.8 ± 2.9 versus 3.4 ± 2.2 ng/mL, P = 0.03). There was also a significant correlation between serum ALT and TLR-2 (r = 0.46; P = 0.01). Docking results illustrated residues within the N-terminus of truncated HBeAg and TLR2, which might facilitate the interaction of these proteins. These findings showed the dominance of G1896A pre-core mutation of HBV variants in this community which was correlated with serum TLR2. Moreover TLR2 is critical for induction of inflammatory cytokines and therefore ALT elevation.

show abstract

“…Chronic infections with blood-borne pathogens, such as HIV-1, HBV and HCV, tend to increase the development of memory homeostasis T cells (Carotenuto et al, 2011; Cao et al, 2014; Cillo et al, 2014; Baskic et al, 2017). During primary viral infections, virus-specific T cell responses are vigorous; however, once a persistent infection is established, both virus-specific CD4 + and CD8 + T cells become dysfunctional or difficult to detect ex vivo (Cao et al, 2014).…”

Section: Ccr7 Is Required For the Sufficient Migration Of Mature Dendmentioning

confidence: 99%

CCL19 and CCR7 Expression, Signaling Pathways, and Adjuvant Functions in Viral Infection and Prevention

Yan

Chen

Wang

et al. 2019

Front. Cell Dev. Biol.

120

104

View full text Add to dashboard Cite

Chemokine (C–C motif) ligand 19 (CCL19) is a critical regulator of the induction of T cell activation, immune tolerance, and inflammatory responses during continuous immune surveillance, homeostasis, and development. Migration of CC-chemokine receptor 7 (CCR7)-expressing cells to secondary lymphoid organs is a crucial step in the onset of adaptive immunity, which is initiated by a complex interaction between CCR7 and its cognate ligands. Recent advances in knowledge regarding the response of the CCL19-CCR7 axis to viral infections have elucidated the complex network of interplay among the invading virus, target cells and host immune responses. Viruses use various strategies to evade or delay the cytokine response, gaining additional time to replicate in the host. In this review, we summarize the impacts of CCL19 and CCR7 expression on the regulation of viral pathogenesis with an emphasis on the corresponding signaling pathways and adjuvant mechanisms. We present and discuss the expression, signaling adaptor proteins and effects of CCL19 and CCR7 as these molecules differentially impact different viral infections and viral life cycles in host homeostatic strategies. The underlying mechanisms discussed in this review may assist in the design of novel agents to modulate chemokine activity for viral prevention.

show abstract

Reciprocal Changes of Naïve and Effector/Memory CD8⁺ T Lymphocytes in Chronic Hepatitis B Virus Infection

Cited by 5 publications

References 26 publications

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation

CCL19 and CCR7 Expression, Signaling Pathways, and Adjuvant Functions in Viral Infection and Prevention

Contact Info

Product

Resources

About

Reciprocal Changes of Naïve and Effector/Memory CD8+ T Lymphocytes in Chronic Hepatitis B Virus Infection

Cited by 5 publications

References 26 publications

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

The Possible Role of TLR2 in Chronic Hepatitis B Patients with Precore Mutation

CCL19 and CCR7 Expression, Signaling Pathways, and Adjuvant Functions in Viral Infection and Prevention

Contact Info

Product

Resources

About

Reciprocal Changes of Naïve and Effector/Memory CD8⁺ T Lymphocytes in Chronic Hepatitis B Virus Infection