Ethnomedicinal products in the development of anti-herpesvirus agents
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Table 1. Members of Human Herpesviridae.
cell protein (ICP) 0 and 4, (iii) early (β1, β2) genes including DNA polymerase and thymidine kinase, (iv) late genes (γ1, γ2) containing glycoprotein B (gB), C (gC), ICP5, and (v) unpaired DNA replication [Sandri-Goldin, 2006]. During symptomatic infection, infected cells transcribe lytic viral genes, but sometimes a small number of latency associated transcript (LAT) genes accumulate, which help the virus to persist in the host cell indefinitely. The primary infection is a self-limited period of illness, but long-term latency is symptom-free. Following reactivation, transcription of viral genes switches from LAT to multiple lytic genes that lead to enhanced replication and virion production. Herpesviruses cause localized skin infections of the mucosal epithelia of the oral cavity, pharynx, oesophagus and the eye, or genitals, depending upon the type involved [Habif, 2004]. Moreover, the herpesvirus establish latent infections that can be periodically reactivated, and sometimes produce serious infections of the central nervous system like acute encephalitis and meningitis, and can be fatal in immune deficient patients [Sandri-Goldin, 2006]. The immediate-early genes of HSV can also activate the genes of HIV [Ostrove et al., 1987], varicella-zoster virus [Felser et al., 1988] or human papillomavirus type 18 [Gius & Laimins, 1989], causing a significant risk factor for transmission of HIV/AIDS [Corey et al., 2004]. The herpesvirus can also lead to scarification, a major cause of blindness in developing nations [Habif, 2004; Sandri-Goldin, 2006]. Moreover, the HSV-2 is also known as an oncogenic virus as it can convert infected cells into tumor cells [Habif, 2004]. The search for selective antiherpesvirus agents is an urgent need as the problems like viral resistance, conflicting efficacy in recurrent infection and immunocompromised patients with available antiherpes drugs remain unresolved. Moreover, herpesviruses (HSV-1 and HSV-2) spread silently (asymptomatic), cause opportunistic infections in immunocompromised (especially cancer and HIV infected) patients, and develop resistance to acyclovir.