We are famili ar with herpesviruses, because most of us have suffered their infection. Herpesviruses are associated with multiple human disorders, ranging from mild symptoms such as cold sores to more severe diseases, such as cancers. For instance, oral herpes is caused by herpes simplex virus type 1 (HSV-1). Here, HSV-1, a prototype of human alpha-herpesvirus, will be mainly described. Besides HSV-1, human cytomegalovirus (HCMV), a prototype of beta-herpesvirus, and Epstein Barr virus (EBV), a prototype of gamma-herpesvirus.
1. Herpesvirus -the term “herpes” is derived from Greek word for “creep=latent or chronic”-herpin.
2. Epstein-Barr virus (EBV)- a human gamma-herpesvirus that is associated with Burkitt’s lymphoma. The virus was named after two scientists who discovered: Dr. Epstein and Dr. Barr.
3. Tumor virus-five human viruses, including EBV and KSHV, are known to be an etiologic agent for human cancer.
Eight species of human herpesviruses have been discovered. Human herpesviruses are divided into three genera: alpha-, beta-, and gamma-herpesviruses.
In alpha-herpesviruses, three species are reported:
(1) herpes simplex virus type 1 (HSV-1), which causes cold sores or oral herpes
(2) herpes simplex virus type 2 (HSV-2), which causes genital herpes
(3) Varicella-Zoster virus (VZV), which causes chicken pox in children and shingles in adults.
Beta-herpesviruses include human cytomegalovirus (HCMV), which causes cytomegalic inclusion disease, and human herpesvirus 6 and 7, which cause roseola.
In gamma-herpesviruses, two species are reported: Epstein-Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV). EBV is associated with two types of human cancers:
Burkitt’s lymphoma and nasopharyngeal carcinoma. KSHV is associated with Kaposi’s sarcoma in AIDS patients. These human gamma-herpesviruses are tumor viruses.In addition, human herpesviruses are systemically named by the
order of discovery, from HHV-1 to HHV-8.
THE LIFE CYCLE OF HSV-1
Cell tropism: HSV-1 infects the epithelium of the mucosal layer. Following primary infection, HSV-1 invades the central nerve system (CNS) via sensory neurons and finally establishes latent infection in nerve ganglia.Similar to other DNA viruses, the virus life cycle can be divided into two phases by the onset of viral genome replication: early phase and late phase. The viral genome replication occurs in the nucleus of infected cells.
Patterns of Virus Infection
Outcomes of virus infection mainly rely on host immune response to virus infection. Depending on the extent of viral replication and pathogenesis during the course of infection, the pattern of viral infection can be divided into four kinds. First, depending on the viral persistence following primary infection, virus infection can be divided into two patterns: transient infection and persistent infection. In clinical circumstance, the former is often termed “acute infection,” while the latter is termed “chronic infection.” Acute infection refers as a viral infection limited by host immune response. Following primary infection, viruses are cleared from the body. Influenza virus and rotavirus infection are two representative examples. In contrast, chronic infection refers to a viral infection that evades host immune response and maintains viral replication for long periods. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are two representative examples. On the other hand, there are cases, where viral replication discontinuously occurs without clearance after primary infection. Depending on viral persistency, this discontinuous infection can be further divided into latent infection or slow infection. In the case of latent infection, viral replication occurs transiently during primary infection. Soon after, the virus stops replicating and becomes undetectable even in the circulating bloodstream, a period dubbed “viral latency.” During latency, the viral genome is maintained without being eliminated and occasionally, the virus resumes its replication by a process termed “reactivation.” Herpesvirus infection, such as HSV-1, is a representative of latent infection. The pattern of slow infection is similar to that of latent infection, but differs in that infection pathology becomes evident following long periods (ie, decades) of infection. Human immunodeficiency virus (HIV) infection is a representative of slow infection.
The Clinical Application of Ozonetherapy for Herpetic Infections and Herpes Zoster
Herpetic infections are painful, depressing diseases and particularly those due to HSV-I and HSV-II are recurrent. They cannot be underestimated because they procure a very poor quality of life. It appears that both herpetic infections and the fearful HZ with the possible combination of PHN can be treated reasonably well with either antiviral drugs or ozonetherapy. However, for the many patients, who suffer more or less frequently of these affections, this is an unsatisfactory information because they only want to know which is the most rapid and effective treatment. It would be a great advancement if we could programme a comparative study including three arms: antivirals, ozonetherapy and both. Such a huge study involves hundreds of patients, many clinicians and great resources for various analyses and it is beyond our possibility. Only imaginative public-health leaders could undertake this endeavour but do they exist?
Meantime the solution that may yield the best and lasting result (if not the cure) can be obtained by COMBINING the orthodox antiviral agents with ozonated major plus minor autohaemotherapy and topical application of ozonated oil. Genital herpes is the infection that often causes severe psychological effects and the majority of patients feel devastated when they learn the diagnosis. This is the reason why we strongly recommend a combination therapy carried out for a prolonged period and likely to reduce recurrency and the risk of transmission.