Induction of IgA and sustained deficiency of cell proliferative response in chronic hepatitis C.
OBJECTIVE
In the present study, antibody and peripheral blood mononuclear cells (PBMC) proliferative responses against hepatitis C virus (HCV) antigens were evaluated in HCV chronically infected patients.


METHODS
Paired serum and PBMC samples were taken six months apart from 34 individuals, either treated or not, and tested by enzyme-linked immunosorbent assay (ELISA) and carboxyfluorescein succinimidyl ester staining.


RESULTS
Over 70% of the patients showed specific IgG and IgM against capsid, E1 and NS3, while HVR-1 was recognized by half of the patients. An increase in the levels of the anti-capsid IgM (P = 0.027) and IgG (P = 0.0006) was observed in six-month samples, compared to baseline. Similarly, a significantly higher percent of patients had detectable IgA reactivity to capsid (P = 0.017) and NS3 (P = 0.005) after six months, compared to baseline. Particularly, IgA against structural antigens positively correlated with hepatic damage (P = 0.036). IgG subclasses evaluation against capsid and NS3 revealed a positive recognition mediated by IgG1 in more than 80% of the individuals. On the contrary, less than 30% of the patients showed a positive proliferative response either of CD4+ or CD8+ T cells, being the capsid poorly recognized.


CONCLUSIONS
These results confirm that while the cellular immune response is narrow and weak, a broad and vigorous humoral response occurs in HCV chronic infection. The observed correlation between IgA and hepatic damage may have diagnostic significance, although it warrants further confirmation.
Amador-Cañizares
Yalena
Y
HCV Department, Vaccine Division, Centro de Ingeniería Genética y Biotecnología, Ave 31, 58 and 190, Playa, P.O. Box 6162, Havana, Cuba. yalena.amador@cigb.edu.cu
Alvarez-Lajonchere
Liz
L
Guerra
Ivis
I
Rodríguez-Alonso
Ingrid
I
Martínez-Donato
Gillian
G
Triana
Julián
J
González-Horta
Eddy E
EE
Pérez
Angel
A
Dueñas-Carrera
Santiago
S
D000328:Adult; D000917:Antibody Formation; D000998:Antiviral Agents / Q000627:therapeutic use; D036022:Capsid Proteins / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D005260:Female; D016174:Hepacivirus / Q000187:drug effects / Q000276:immunology*; D018937:Hepatitis C Antibodies / Q000097:blood*; D018936:Hepatitis C Antigens / Q000276:immunology*; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood*; D016898:Interferon-alpha / Q000627:therapeutic use; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology* / Q000821:virology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012254:Ribavirin / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000276:immunology / Q000821:virology; D015854:Up-Regulation; D014759:Viral Envelope Proteins / Q000276:immunology; D017361:Viral Nonstructural Proteins / Q000276:immunology; D012697:Serine Endopeptidases; D043583:Nucleoside-Triphosphatase; D053487:DEAD-box RNA Helicases; D000085242:Viral Proteases
D000998:Antiviral Agents; D036022:Capsid Proteins; D018937:Hepatitis C Antibodies; D018936:Hepatitis C Antigens; D007070:Immunoglobulin A; D016898:Interferon-alpha; D012254:Ribavirin; D014759:Viral Envelope Proteins; D017361:Viral Nonstructural Proteins; C087035:E1 protein, Hepatitis C virus; C084422:NS3 protein, hepatitis C virus; D012697:Serine Endopeptidases; D043583:Nucleoside-Triphosphatase; D053487:DEAD-box RNA Helicases; D000085242:Viral Proteases