Hsp BP 1 and anti‐Hsp BP 1 levels in the serum of HIV ‐infected individuals are associated to the disease progression

Abstract

Aims The objective of this research was to quantify the levels of circulating HspBP1 and anti‐HspBP1 IgG in HIV‐infected individuals and to correlate them with CD4 T cell counts and viral load, as well as to determine the kinetics of those proteins during acute phase. Methods and Results Sixty serum samples from HIV‐positive outpatients, thirty with high viral load and thirty with low viral load were analysed. The HspBP1 and anti‐HspBP1 were quantified by ELISA. To investigate the kinetic of HspBP1 and anti‐HspBp1 during the acute phase, these proteins and antibodies were quantified in samples of a commercial seroconverting HIV panel. All dosages were compared with the CD4 and CD8 T cell counts and HIV viral load. The results indicated that HIV positive outpatients presented significant increase in HspBP1 and anti‐HspBP1 serum levels, compared with uninfected healthy. HspBP1 and anti‐HspBP1 were negatively correlated with CD4 counts and CD4:CD8 ratio. In the acute phase, HspBP1 became significantly elevated 15 days after HIV infection. Conclusions These results indicate that the quantification of HspBP1 can be associated to others well‐established parameters of the HIV progression. Significance and Impact of the Study The discovery that HspBp1 and anti‐HspBp1 are associated with progression of HIV infection is new and corroborates to validate the quantification of these proteins as an additional strategy in the management of the HIV infection.

Detection of Anti-IgGs against Heat Shock Proteins 27 and 20, HP91 Peptide, and HIV-1 Polypeptides in HIV-Positive and Negative Patients

“…HspBP1 and anti-HspBP1 negatively correlated with CD4 counts. In the acute phase, HspBP1 was significantly increased 15 days after HIV infection [35]. Our previous study showed that overexpression of Hsp27, similar to Hsp20, significantly decreased herpes simplex virus-1 (HSV-1) replication, but it did not affect the replication of human immunodeficiency virus-1 (HIV-1) and hepatitis C virus (HCV) in vitro.…”