Author:
Rakityanskaya Irina Anisimovna,Ryabova Tatiana Sergeevna,Kalashnikova Anastasia Andreevna
Abstract
Objective. To evaluate the efficiency of allokin-alpha therapy on the level of isolation of Epstein-Barr virus (EBV) and herpes simplex virus type 6 (HHV-6) DNA copy numbers in saliva samples, on the time course of changes in the production of IFN-α and IFN-γ and on that of clinical complaints in patients with chronic fatigue syndrome in the presence of chronic EBV and HHV-6 infections. Subjects and methods. A total of 53 patients (36 women and 17 men) with with chronic fatigue syndrome in the presence of chronic herpesvirus infection were examined; the patients’ their mean age was 34.51 ± 1.74 years. All the patients underwent determination of the amount of EBV and HHV-6 DNA in their saliva samples by polymerase chain reaction (PCR) and the blood levels of IFN-α and IFN-γ, and the spontaneous and induced production of these cytokines in the blood lymphocyte cultures. All the patients received allokin-alpha therapy with 9 subcutaneous injections of 1.0 mg every other day. The patients were divided into three groups: 1) 26 patients with chronic EBV infection; 2) 18 patients with EBV + HHV-6 co-infection; 3) 9 patients with HHV-6 infection. Results. After allokin-alpha therapy, in Group 1 EBV DNA was PCR negative in 57.69% of patients; in Group 3, that was positive in all patients. In Group 2, EBV and HHV-6 DNA was found to be absent in 44.44 and 5.55% of patients, respectively. In all the groups, the serum and spontaneous production of IFN-α did not change significantly one month after the end of therapy. The level of induced IFN-α tended to decrease. IFN-γ production also tended to reduce in all the groups. After the end of therapy, the patients in all the groups showed a significant decline in the number of clinical complaints. Conclusion. The efficiency of allokin-alpha therapy varies in patients with chronic herpesvirus infection and depends upon virus type. The greatest efficacy of the drug was found in patients with EBV infection.
Reference43 articles.
1. Cuomo L., Angeloni A., Zompetta C., Cirone M., Calogero A., Frati L., Ragona G., Faggioni A. Human herpesvirus 6 variant A, but not variant B, infects EBV-positive B lymphoid cells, activating the latent EBV genome through a BZLF-1-dependent mechanism. AIDS Res. Hum. Retrovir. 1995; (11): 1241-5.
2. Flamand L., Menezes J. Cyclic AMP-responsive element- dependent activation of Epstein-Barr virus zebra promoter by human herpesvirus 6. J. Virol. 1996; 70(3): 1784-91.
3. Flamand L., Stefanescu L.I., Ablashi D.V., Menezes J. Activation of the Epstein-Barr virus replicative cycle by human herpesvirus 6. J. Virol. 1993; 67: 6768-77.
4. Bertram G.N., Dreiner G.R., Krueger A., Ramon D.V., Ablashi S., Salahuddin Z., Balachandram N. Frequent double infection with Epstein-Barr virus and human herpesvirus-6 in patients with acute infectious mononucleosis. In Vivo 1991; (5): 271-27.
5. Pellett P.E., Ablashi D.V., Ambros P.F., Agut H., Caserta M.T., Descamps V. et al. Chromosomally integrated human herpesvirus 6: questions and answers. Rev. Med. Virol. 2012; 22(3): 144-55. DOI: 10.1002/ rmv.715.