VIRUS REPLICATION – AN INTRODUCTION

Abstract

Viruses can only multiply in an internal cellular environment. They lack subcellular organelles such as nuclei, mitochondria, ribosomes as well as cytoplasmic components that are necessary for the synthesis of their own structural components: nucleic acids (RNA or DNA), proteins, carbohydrates and lipids. Thus, viruses cannot multiply but must be replicated by the cells that they invade. The essential steps of virus replication are similar for all virus classes: first, a virus particle (virion) must attach to the outer surface of the host cell. Next, it penetrates the cell membrane and enters the cytoplasmic environment. Some or all of the outer surface layers of the virus (envelope and capsid) are removed, so that the viral genome (DNA or RNA) becomes accessible to the cellular organelles and enzymes which will initiate the replication process. Some of the genetic information is used to synthesize virus-specific enzymes (polymerases) which are necessary for the replication of the viral nucleic acid. Other parts of the viral genome code for the structural proteins. The newly synthesized viral nucleic acid and proteins are then assembled (maturation) into new viral particles which may leave the cells either by simple cell lysis or by a budding process at the membranes of the outer cell surface or in the endoplasmic reticulum. This basic strategy of virus infections leaves ample space for variations depending on whether the viral genome is composed of DNA or RNA, on whether it is double- or single-stranded, linear or circular, monolithic or fragmented. The parental RNA may either be directly used by ribosomes (+ strand viruses), or it may first need transcription into a complementary strand (- strand viruses). Enveloped viruses probably require the synthesis of specific carbohydrates and lipids. Depending on the genetic make-up of the host cell and on the conditions of infection, the virus cycle may be productive (i.e. many new infectious particles are released by each infected cell) or it may be restrictive, or even abortive.Some viruses may remain latently present in cells over a long time and over a large number of generations. Several mechanisms for such chronicity of virus infection have been discovered. Certain taxa of viruses have the unique capability to integrate their genome, or a fragment thereof, into that of the cell. Chronic infections may also be maintained by the generation of defective-interfering (DI) particles, which contain only part of the virus genome, but which are replicated when they are present in cells, along with complete virus particles. In general the small size of the DI-genome allows it to be replicated more rapidly than the intact genome and hence competes strongly for the polymerases. In certain conditions, DI-particles can alter the lytic pathway of infection and rapidly establish persistent infections in which the cells survive but carry in them considerable amounts of virus antigens. This is an important area in virology to-day as it may be related to the development of long-term degenerative diseases which may have a viral etiology.