scholarly journals Constraints on HIV-1 evolution and immunodominance revealed in monozygotic adult twins infected with the same virus

2006 ◽  
Vol 203 (3) ◽  
pp. 529-539 ◽  
Author(s):  
Rika Draenert ◽  
Todd M. Allen ◽  
Yang Liu ◽  
Terri Wrin ◽  
Colombe Chappey ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Viral Infections ◽  
Immune Escape ◽  
Monozygotic Twins ◽  
T Cell Response ◽  
Envelope Gene ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Cell Counts

The predictability of virus–host interactions and disease progression in rapidly evolving human viral infections has been difficult to assess because of host and genetic viral diversity. Here we examined adaptive HIV-specific cellular and humoral immune responses and viral evolution in adult monozygotic twins simultaneously infected with the same virus. CD4 T cell counts and viral loads followed similar trajectories over three years of follow up. The initial CD8 T cell response targeted 17 epitopes, 15 of which were identical in each twin, including two immunodominant responses. By 36 months after infection, 14 of 15 initial responses were still detectable in both, whereas all new responses were subdominant and remained so. Of four responses that declined in both twins, three demonstrated mutations at the same residue. In addition, the evolving antibody responses cross-neutralized the other twin's virus, with similar changes in the pattern of evolution in the envelope gene. These results reveal considerable concordance of adaptive cellular and humoral immune responses and HIV evolution in the same genetic environment, suggesting constraints on mutational pathways to HIV immune escape.

scholarly journals TRAF6 Is Required for Generation of the B-1a B Cell Compartment as well as T Cell-Dependent and -Independent Humoral Immune Responses

PLoS ONE ◽  
2009 ◽  
Vol 4 (3) ◽  
pp. e4736 ◽  
Author(s):  
Takashi Kobayashi ◽  
Tae Soo Kim ◽  
Anand Jacob ◽  
Matthew C. Walsh ◽  
Yuho Kadono ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
B Cell ◽  
Cell Compartment ◽  
Humoral Immune ◽  
Humoral Immune Responses

Control of Cellular and Humoral Immune Responses by Peptides Containing T-cell Epitopes

1989 ◽  
Vol 54 (0) ◽  
pp. 497-504 ◽  
Author(s):  
M.T. Scherer ◽  
B.M.C. Chan ◽  
F. Ria ◽  
J.A. Smith ◽  
D.L. Perkins ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
T Cell Epitopes ◽  
Humoral Immune ◽  
Humoral Immune Responses

BCG vaccine elicits both T-cell mediated and humoral immune responses directed against mycobacterial lipid components

Vaccine ◽  
2006 ◽  
Vol 24 (29-30) ◽  
pp. 5700-5707 ◽  
Author(s):  
Yoshiyuki Watanabe ◽  
Eiji Watari ◽  
Isamu Matsunaga ◽  
Kenji Hiromatsu ◽  
Christopher C. Dascher ◽  
...  
Keyword(s):  
T Cell ◽  
Immune Responses ◽  
Bcg Vaccine ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Lipid Components

scholarly journals Targeted Inactivation of the Tetraspanin CD37 Impairs T-Cell-Dependent B-Cell Response under Suboptimal Costimulatory Conditions

2000 ◽  
Vol 20 (15) ◽  
pp. 5363-5369 ◽  
Author(s):  
Klaus-Peter Knobeloch ◽  
Mark D. Wright ◽  
Adrian F. Ochsenbein ◽  
Oliver Liesenfeld ◽  
Jürgen Löhler ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Viral Infections ◽  
Cell Interactions ◽  
Antibody Responses ◽  
Cellular Activation ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Targeted Inactivation ◽  
Deficient Mice

ABSTRACT CD37 is a membrane protein of the tetraspanin superfamily, which includes CD9, CD53, CD63, CD81, and CD82. Many of these molecules are expressed on leukocytes and have been implicated in signal transduction, cell-cell interactions, and cellular activation and development. We generated and analyzed mice deficient for CD37. Despite the high expression of CD37 on cells of the immune system, no changes in development and cellular composition of lymphoid organs were observed in mice lacking CD37. Analyses of humoral immune responses revealed a reduced level of immunoglobulin G1 (IgG1) in the sera of nonimmunized mice and an alteration of responses to T-cell-dependent antigens. Antibody responses to model antigen administered in the absence of adjuvant and to viral infections were generally poor in CD37-deficient mice. These poor antibody responses could be overcome by the immunization of antigen together with adjuvant. These results suggest a role for CD37 in T-cell–B-cell interactions which manifests itself under suboptimal costimulatory conditions.

scholarly journals Evolutive Temporal Footprint of an HIV-1 Envelope Protein in an Epidemiologically Linked Cluster

2020 ◽  
Vol 14 (1) ◽  
pp. 41-49
Author(s):  
Elidamar Nunes de Carvalho Lima ◽  
Rodrigo Sucupira Andrade Lima ◽  
Muhammad Shoaib Arif ◽  
José Roberto Castilho Piqueira ◽  
Ricardo Sobhie Diaz
Keyword(s):  
Amino Acids ◽  
Viral Load ◽  
T Cell ◽  
Information Entropy ◽  
Envelope Protein ◽  
Immune Escape ◽  
Envelope Gene ◽  
Cell Counts ◽  
Hiv 1 ◽  
Over Time

Background: The C2V3C3 region of gp 120, encoded by the HIV-1 envelope gene (env), is an important antigenic target, a key determinant for viral evolution and essential for determining epitopes for vaccines. Methods: The relationships among genetic sequence diversity, selective pressure, constraints on HIV-1 envelope protein were explored and also correlated this analysis with information entropy; hypermutation; HIV tropism; CD4+ T cell counts or HIV viral load. A total of 179 HIV-1 C2V3C3 sequences derived from cell-free plasma were used, determined from serial samples, in four epidemiologically linked individuals (one infected blood donor, two transfusion recipients and a sexual partner infected by one of the recipients) over a maximum period of 8 years. This study is important because it considers the analysis of patterns in genomic sequences, without drugs and over time. Results: A temporal relationship among information entropy, hypermutation, tropism switch, viral load, and CD4+ T cell count was determined. Changes in information entropy were time-dependent, and an increase in entropy was observed in the C2V3C3 region at amino acids G313 and F317-I320 (related to the GPGR-motif and coreceptor tropism), and at amino acids A281 in C2 and A346 in C3, related to immune escape. Conclusion: The increase of information entropy over time was correlated with hypermutation and the emergence of nonR5- strains, which are both associated with more variable genomes.

scholarly journals Recombinant Rabies Virus Overexpressing OX40-Ligand Enhances Humoral Immune Responses by Increasing T Follicular Helper Cells and Germinal Center B Cells

Vaccines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 144 ◽  
Author(s):  
Yingying Li ◽  
Ling Zhao ◽  
Baokui Sui ◽  
Zhaochen Luo ◽  
Yachun Zhang ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Immune Responses ◽  
Rabies Virus ◽  
Germinal Center ◽  
Rabies Vaccine ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Follicular Helper ◽  
Ox40 Ligand

Rabies, caused by the rabies virus (RABV), remains a serious threat to public health in most countries. Development of a single-dose and efficacious rabies vaccine is the most important method to restrict rabies virus transmission. Costimulatory factor OX40-ligand (OX40L) plays a crucial role in the T cell-dependent humoral immune responses through T-B cell interaction. In this work, a recombinant RABV overexpressing mouse OX40L (LBNSE-OX40L) was constructed, and its effects on immunogenicity were evaluated in a mouse model. LBNSE-OX40L-immunized mice generated a larger number of T follicular helper (Tfh) cells, germinal center (GC) B cells, and plasma cells (PCs) than the parent virus LBNSE-immunized mice. Furthermore, LBNSE-OX40L induced significantly higher levels of virus-neutralizing antibodies (VNA) as early as seven days post immunization (dpi), which lasted for eight weeks, resulting in better protection for mice than LBNSE (a live-attenuated rabies vaccine strain). Taken together, our data in this study suggest that OX40L can be a novel and potential adjuvant to improve the induction of protective antibody responses post RABV immunization by triggering T cell-dependent humoral immune responses, and that LBNSE-OX40L can be developed as an efficacious and nonpathogenic vaccine for animals.

T Cell Proliferative Responses and IgG Antibodies to β2GPI in Patients with Diabetes and Atherosclerosis

2020 ◽  
Vol 20 ◽  
Author(s):  
Mohammad Rafiee Monjezi ◽  
Hamed Fouladseresht ◽  
Shirin Farjadian ◽  
Behrouz Gharesi-Fard ◽  
Shahdad Khosropanah ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Immune Responses ◽  
Igg Antibody ◽  
Group Iii ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Group I ◽  
Diabetes Status ◽  
Patients With Diabetes

Background: Diabetes increases the risk of myocardial infarction (MI) by 2 to 3 folds. T-lymphocytes play a role in atherosclerosis, which is the main pathology behind MI. Cellular immune responses to beta-2 glycoprotein I (β2GPI) are shown in carotid atherosclerosis. Objective: To investigate the self-reactive, β2GPI-specific T-lymphocytes in patients with and without diabetes and atherosclerosis. Methods: Collectively, 164 subjects with and without diabetes that underwent coronary angiography were divided into four groups based on their diabetes status and coronary stenosis. Group I=Diabetic with ≥50% stenosis: A+D+ (n=66); Group II=Nondiabetic with ≥50% stenosis, A+D- (n=39); Group III=Diabetic with <50% stenosis: A-D+ (n=28); and Group IV=Non-diabetic with <50% stenosis: A-D- (n=31). All groups were evaluated for anti-β2GPI IgG antibody by ELISA method. Then, PBMCs were isolated from 18 subjects and were stimulated with β2GPI-derived peptides to assess their proliferation in accordance with their HLA-DRB1 alleles. Results: Mean β2GPI IgG levels were higher in groups with ≥50% stenosis (A+) compared to those with <50% stenosis (A-), (P=0.02(. Co-presence of diabetes in A+ individuals increased mean β2GPI-specific IgG. Auto-reactive β2GPI-specific T cells were detected in the repertoire of T-lymphocytes in all groups. β2GPI-peptides showed promiscuous restriction by various HLADRB1. Conclusion: β2GPI is the target of cellular and humoral immune responses in patients with atherosclerosis. Since the T cell responses but not antibodies were detectable in A-D+ and A-D- groups, it is reasonable to assume that cellular responses preceded the humoral responses. Post-translation modifications of β2GPI under oxidative and glycemic stresses may have increased the IgG levels in patients with diabetes. Finally, identification of antigens that trigger immuno-pathogenesis in atherosclerosis and diabetes may help development of immunomodulation methods to prevent or treat these debilitating diseases.

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