The unique properties of viruses set them apart from living creatures. Viruses lack many of the attributes of cells, including the ability to self-replicate. Only when it infects a cell does a virus acquire the key attribute of a living system— reproduction. Viruses are known to infect a wide variety of plant and animal hosts as well as protists, fungi, and bacteria. However, most viruses are restricted to infecting specific types of cells of only one host species, a property known as “tropism”. Recently, viruses called virophages have been discovered that infect other viruses. Host–virus interactions tend to be highly specific, and the biologic range of viruses mirrors the diversity of potential host cells. Further diversity of viruses is exhibited by their broad array of strategies for replication and survival.

Viral particles are generally small (eg, adenovirus has a diameter of 90 nm) and consist of a nucleic acid molecule, either DNA or RNA, enclosed in a protein coat, or capsid (sometimes itself surrounded by an envelope of lipids, proteins, and carbohydrates). Proteins—frequently glycoproteins— comprising the capsid and/or making up part of the lipid envelope (e.g., HIV gp120) determine the specificity of inter action of a virus with its host cell. The capsid protects the nucleic acid cargo. The surface proteins, whether they are externally exposed on the capsid or associated with the envelope facilitates attachment and penetration of the host cell by the virus. Once inside the cell, viral nucleic acid redirects the host’s enzymatic machinery to functions associated with replication and assembly of the virus. In some cases, genetic information from the virus can be incorporated as DNA into a host chromosome (a provirus). In other instances, the viral genetic information can serve as a basis for cellular manufacture and release of copies of the virus. This process calls for replication of the viral nucleic acid and production of specific viral proteins. Maturation consists of assembling newly synthesized nucleic acid and protein subunits into mature viral particles, which are then liberated into the extracellular environment. Some very small viruses require the assistance of another virus in the host cell for their replication. The delta agent, also known as hepatitis D virus (HDV), has a RNA genome that is too small to code for even a single capsid protein (the only HDV-encoded protein is delta anti gen) and needs help from hepatitis B virus for packaging and transmission.

Some viruses are large and complex. For example, Mimi virus, a DNA virus infecting Acanthamoeba, a free-living soil ameba, has a diameter of 400–500 nm and a genome that encodes 979 proteins, including the first four aminoacyl tRNA synthetases ever found outside of cellular organisms. This virus also encodes enzymes for polysaccharide biosynthesis, a process typically performed by the infected cell. An even larger marine virus has recently been discovered (Megavirus); its genome (1,259,197-bp) encodes 1120 putative proteins and is larger than that of some bacteria (see Table 1). Because of their large size, these viruses resemble bacteria when observed in stained preparations by light microscopy; however, they do not undergo cell division or contain ribosomes.

Table1. Comparison of Genome Sizes in Selected Prokaryotes, Bacteriophages, and Viruses

Several transmissible plant diseases are caused by viroids—small, single-stranded, covalently closed circular RNA molecules existing as highly base-paired rod-like structures. They range in size from 246 to 375 nucleotides in length. The extracellular form of the viroid is naked RNA— there is no capsid of any kind. The RNA molecule contains no protein-encoding genes, and the viroid is therefore totally dependent on host functions for its replication. Viroid RNA is replicated by the DNA-dependent RNA polymerase of the plant host; preemption of this enzyme may contribute to viroid pathogenicity.

The RNAs of viroids have been shown to contain inverted repeated base sequences (also known as insertion sequences) at their 3′ and 5′ ends, a characteristic of transposable elements  and retroviruses. Thus, it is likely that they have evolved from transposable elements or retroviruses by the deletion of internal sequences.

مواضيع ذات صلة

Human Cytomegalovirus

Influenza Virus Infections in Humans

Varicella-Zoster Virus

Adenovirus Coinfection with SARS-CoV-2

Genetic Polymorphisms susceptibility to SARS-CoV-2

Acute viral hepatitis

Human receptor of coronavirus and Adenovirus

Antiviral Chemotherapy

Humoral Immune Responses to SARS-CoV-2 Infection

Cellular Immune Responses to SARS-CoV-2

Pathogenesis of SARS-CoV-2

Epidemiology of SARS-CoV-2