To truly understand the herpes virus is helpful to first gain some knowledge on viruses in general. Viruses are the smallest known microbes, or infectious agents which medical science has discovered to date. Most viruses consist of a nucleic acid surrounded by a protein known layer as the capsid; The complex protein-nucleic acid is considered nucleocapsid. For more complex virus such as herpes virus, the nucleocapsid is surrounded by a structure similar to a membrane which contains carbohydrates, lipids and proteins. Each virus contains two major complex chemicals that contain the genetic code of the virus serving as a model to make more virus. To multiply, a virus must enter a living cell, remove the cellular protein layer and then use the RNA or DNA of the cells that synthesize redirect mechanism to make more copies of the virus. This process of manufacturing new viruses can actually destroy or damage living cells or "host". If the host cells are sufficient to be damaged or destroyed resulting in a viral disease such as influenza (flu) or genital herpes viral diarrhea. Each virus has adapted to infect a particular cell type in a specific living organism which is why there are so many types of viruses. Because become so specialized some viruses can infect certain cell types, e.g., liver cells or muscle cells or brain cells, leaving other cells alone. Similarly, many viruses are still limited to the type of species that can infect. The term "herpes virus" refers to any member of the family of type 1 herpes virus and herpes simplex type 2 necleocapsid simplex herpes virus is surrounded by an envelope containing structures spikes extending from the surface and which contains the DNA. So far, scientists have identified more than 115 different herpesviruses and found more than 50 different species of animals that can be infected by a type of herpes virus. Human beings seem to be a natural reservoir for at least 8 different types of herpes virus that normally distributed from human to human and do not usually cause disease in other animals.
Protruding from the outer surface of the herpes virus is a carbohydrate, protein structures called glycoproteins. Glycoproteins allow virus entry initially proteoglycans, which are complex chemical structures on the surface of living cells. After fixing of the host cell, then glycopoteins interact with cell surface structures to cause changes in the cytoskeletal structure of cell membranes. These changes allow the viral envelope to fuse with the plasma membrane of the cell, essentially melt to form a modified cell. When this occurs the fusion, the herpes virus nucleocapsid enters the cytoplasm of the host cell by attaching structures called microtubules and microfilaments which form an internal transport network used for materials moving within the cell skeleton type. With this structure of the DNA of the herpes virus enters the nucleus of the host cell where it makes copies of the viral DNA, which are released from the cell and spread and infect other neighboring cells. This process of generating new viral particles kill the infected host cell.
If the herpes virus is remained in the cells of the skin, where the initial attachment of the virus occurs, it is possible that the immune system can optionally control the infection and release virus in the body. The herpes virus, however, has found a way to hide from the immune system, hibernating in nerve cells. For unknown reasons, the replication process of the herpes virus does not start in a number of cells, instead of hibernation and to establish a latent infection. When the herpes virus is hybernating it is in an inactive state and can not be detected by the immune system. Latency does not cause disease, but unfortunately the latent virus can reactivate and produce more virus, which, in turn, causes recurrent herpes.
Whatever the trigger, after the reactivation, the herpes virus is transported from the body of the nerve cell to nerve endings in the skin where it is released to replicate in cells of the skin. This replication can sometimes cause full blown herpes sores outbreaks, but other times it can result in "load shedding" the virus that does not cause recognizable symptoms.
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