Can anyone explain herpesvirus replication?

Question

Can anyone explain herpesvirus replication?

Answer 1

Binding to the cell surface: As with many other viruses, cell tropism is determined by the availability of the correct receptor on the surface of the cell to be infected. The virus fuses with the cell membrane at ambient pH and so there is the possibility of syncytia formation between infected cells and therefore cell to cell transmission even in the presence of neutralizing humoral antibodies. This means that cell-mediated immunity is important in suppressing herpes virus infections.

Nucleocapsid enters cytoplasm: The tegument-surrounded nucleocapsid is carried to the nuclear membrane where the nucleocapsid binds. The DNA genome then enters the nucleus.

Transcription: This is a very complex process, as might be expected from the large size of genome. There are three classes of proteins that need to be made for the production of a mature virus.

Alpha proteins: These are the immediate-early proteins. They are involved in transcriptional regulation and are not found in the mature virion. They are also involved in the control of beta protein synthesis  



  Stages in the exocytosis of herpes virus from the nucleus, in which the virus core is assembled, to the plasma membrane



Beta proteins. These are the early proteins and are involved also in DNA replication (they include the DNA polymerase and transcription factors). Only a few copies of DNA polymerase need to be made for replication to occur .

Gamma proteins. These are the late proteins and are structural components of the virus. The synthesis of gamma proteins is initiated after the start of DNA synthesis

RNA transcription: The herpes DNA is transcribed to RNA by a cellular enzyme (DNA-dependent RNA polymerase I). However, the transcription of the various genes is dependent on both nuclear factors of the cell AND proteins encoded by the virus. This control of viral mRNA, and therefore, viral protein, synthesis determines whether infection will result in the production of new virus particles and cell death (a lytic infection), persistent shedding of virus (persistent infection) or latency. Whether latency occurs is the property of the host cell, that is some cells do not allow the replication of viral DNA. If the cell permits progression beyond the immediate early genes, a lytic infection will ensue.

DNA synthesis: Herpes viruses encode their own DNA-dependent DNA polymerase. In addition, some herpes viruses encode enzymes (such as thymidine kinase) that allow the virus to grow in non-dividing cells that do not therefore contain the precursors of DNA synthesis. Without this enzyme, neurotropic herpes viruses could not replicate because of the low amounts of certain DNA precursors in nerve cells.

Assembly: Nucleocapsids are assembled in the nucleus and are filled with DNA They then bud through the double nuclear membrane and leave the cell via the exocytosis pathway or they may bud through another cell membrane such as the plasma membrane