following the structure-mediated self-assembly of the virus particles, some modification of the proteins often occurs. in viruses such as hiv, this modification (sometimes called maturation) occurs after the virus has been released from the host cell. release – viruses can be released from the host cell by lysis, a process that kills the cell by bursting its membrane and cell wall if present: this is a feature of many bacterial and some animal viruses. some viruses undergo a lysogenic cycle where the viral genome is incorporated by genetic recombination into a specific place in the host's chromosome. the viral genome is then known as a "provirus" or, in the case of bacteriophages a "prophage". whenever the host divides, the viral genome is also replicated. the viral genome is mostly silent within the host. at some point, the provirus or prophage may give rise to the active virus, which may lyse the host cells. enveloped viruses (e.g., hiv) typically are released from the host cell by budding. during this process, the virus acquires its envelope, which is a modified piece of the host's plasma or other, internal membrane. genome replication the genetic material within virus particles, and the method by which the material is replicated, varies considerably between different types of viruses. dna virusesthe genome replication of most dna viruses takes place in the cell's nucleus. if the cell has the appropriate receptor on its surface, these viruses enter the cell either by direct fusion with the cell membrane (e.g., herpesviruses) or—more usually—by receptor-mediated endocytosis. most dna viruses are entirely dependent on the host cell's dna and rna synthesising machinery and rna processing machinery. viruses with larger genomes may encode much of this machinery themselves. in eukaryotes, the viral genome must cross the cell's nuclear membrane to access this machinery, while in bacteria it need only enter the cell. rna virusesreplication of rna viruses usually takes place in the cytoplasm. rna viruses can be placed into four different groups depending on their modes of replication. the polarity (whether or not it can be used directly by ribosomes to make proteins) of single-stranded rna viruses largely determines the replicative mechanism; the other major criterion is whether the genetic material is single-stranded or double-stranded. all rna viruses use their own rna replicase enzymes to create copies of their genomes. reverse transcribing virusesreverse transcribing viruses have ssrna (retroviridae, metaviridae, pseudoviridae) or dsdna (caulimoviridae, and hepadnaviridae) in their particles. reverse transcribing viruses with rna genomes (retroviruses) use a dna intermediate to replicate, whereas those with dna genomes (pararetroviruses) use an rna intermediate during genome replication. both types use a reverse transcriptase, or rna-dependent dna polymerase enzyme, to carry out the nucleic acid conversion. retroviruses integrate the dna produced by reverse transcription into the host genome as a provirus as a part of the replication process; pararetroviruses do not, although integrated genome copies of especially plant pararetroviruses can give rise to infectious virus. they are susceptible to antiviral drugs that inhibit the reverse transcriptase enzyme, e.g. zidovudine and lamivudine. an example of the first type is hiv, which is a retrovirus. examples of the second type are the hepadnaviridae, which includes hepatitis b virus. cytopathic effects on the host cell the range of structural and biochemical effects that viruses have on the host cell is extensive. these are called 'cytopathic effects'. most virus infections eventually result in the death of the host cell. the causes of death include cell lysis, alterations to the cell's surface membrane and apoptosis. often cell death is caused by cessation of its normal activities because of suppression by virus-specific proteins, not all of which are components of the virus particle. the distinction between cytopathic and harmless is gradual. some viruses, such as epstein–barr virus, can cause cells to proliferate without causing malignancy, while others, such as papillomaviruses, are established causes of cancer. dormant and latent infections some viruses cause no apparent changes to the infected cell. cells in which the virus is latent and inactive show few signs of infection and often function normally. this causes persistent infections and the virus is often dormant for many months or years. this is often the case with herpes viruses. host range viruses are by far the most abundant biological entities on earth and they outnumber all the others put together. they infect all types of cellular life including animals, plants, bacteria and fungi. different types of viruses can infect only a limited range of hosts and many are species-specific. some, such as smallpox virus for example, can infect only one species—in this case humans, and are said to have a narrow host range. other viruses, such as rabies virus, can infect different species of mammals and are said to have a broad range. the viruses that infect plants are harmless to animals, and most viruses that infect other animals are harmless to humans. the host range of some bacteriophages is limited to a single strain of bacteria and they can be used to trace the source of outbreaks of infections by a method called phage typing. the complete set of viruses in an organism or habitat is called the virome; for example, all human viruses constitute the human virome. novel viruses a novel virus is one that has not previously been recorded. it can be a virus that is isolated from its natural reservoir or isolated as the result of spread to an animal or human host where the virus had not been identified before. it can be an emergent virus, one that represents a new virus, but it can also be an extant virus that has not been previously identified. the sars-cov-2 coronavirus that caused the pandemic of covid disease is an example of a novel virus. classification main article: virus classification classification seeks to describe the diversity of viruses by naming and grouping them on the basis of similarities. in 1962, andré lwoff, robert horne, and paul tournier were the first to develop a means of virus classification, based on the linnaean hierarchical system. this system based classification on phylum, class, order, family, genus, and species. viruses were grouped according to their shared properties (not those of their hosts) and the type of nucleic acid forming their genomes. in 1966, the international committee on taxonomy of viruses (ictv) was formed. the system proposed by lwoff, horne and tournier was initially not accepted by the ictv because the small genome size of viruses and their high rate of mutation made it difficult to determine their ancestry beyond order. as such, the baltimore classification system has come to be used to supplement the more traditional hierarchy. starting in 2018, the ictv began to acknowledge deeper evolutionary relationships between viruses that have been discovered over time and adopted a 15-rank classification system ranging from realm to species. additionally, some species within the same genus are grouped into a genogroup. ictv classification the ictv developed the current classification system and wrote guidelines that put a greater weight on certain virus properties to maintain family uniformity. a unified taxonomy (a universal system for classifying viruses) has been established. only a small part of the total diversity of viruses has been studied. as of 2022, 6 realms, 10 kingdoms, 17 phyla, 2 subphyla, 40 classes, 72 orders, 8 suborders, 264 families, 182 subfamilies, 2,818 genera, 84 subgenera, and 11,273 species of viruses have been defined by the ictv. the general taxonomic structure of taxon ranges and the suffixes used in taxonomic names are shown hereafter. as of 2022, the ranks of subrealm, subkingdom, and subclass are unused, whereas all other ranks are in use. realm (-viria) subrealm (-vira) kingdom (-virae) subkingdom (-virites) phylum (-viricota) subphylum (-viricotina) class (-viricetes) subclass (-viricetidae) order (-virales) suborder (-virineae) family (-viridae) subfamily (-virinae) genus (-virus) subgenus (-virus) species baltimore classification the baltimore classification of viruses is based on the method of viral mrna synthesis the nobel prize-winning biologist david baltimore devised the baltimore classification system. the ictv classification system is used in conjunction with the baltimore classification system in modern virus classification. the baltimore classification of viruses is based on the mechanism of mrna production. viruses must generate mrnas from their genomes to produce proteins and replicate themselves, but different mechanisms are used to achieve this in each virus family. viral genomes may be single-stranded (ss) or double-stranded (ds), rna or dna, and may or may not use reverse transcriptase (rt). in addition, ssrna viruses may be either sense (+) or antisense (−). this classification places viruses into seven groups: i: dsdna viruses (e.g. adenoviruses, herpesviruses, poxviruses) ii: ssdna viruses (+ strand or "sense") dna (e.g. parvoviruses) iii: dsrna viruses (e.g. reoviruses) iv:(+)ssrna viruses (+ strand or sense) rna (e.g. coronaviruses, picornaviruses, togaviruses) v: (−)ssrna viruses (− strand or antisense) rna (e.g. orthomyxoviruses, rhabdoviruses) vi: ssrna-rt viruses (+ strand or sense) rna with dna intermediate in life-cycle (e.g. retroviruses) vii: dsdna-rt viruses dna with rna intermediate in life-cycle (e.g. hepadnaviruses) role in human disease