What virus contains rna as its genetic information

Try out PMC Labs and tell us what you think. Learn More. RdRp is the key player for all of these processes. RdRps of all RNA viruses probably arose from a common ancestor. The RdRp and other proteins required for viral genome synthesis are often called the replicase complex.

The replicase complex consists of the set of proteins required to produce infectious genomes. The number of proteins in the replicase complex differs among virus families. There may also be a requirement for host cell proteins. Their genomes are translated shortly after penetration into the host cell to produce the RdRp and other viral proteins required for synthesis of additional viral RNAs.

Positive-strand RNA viruses often use large complexes of cellular membranes for genome replication. They actively modify host cell membranes to construct viral replication scaffolds. For each of these groups of viruses, the first synthetic event after genome penetration is transcription.

This is accomplished by viral proteins including the RdRp that enter cell with the genome. RdRp is the key player for all of these processes Fig. Ribbon diagram of flavivirus RdRp.

Fingers, palm, and thumb subdomains are colored in blue, green, and red, respectively. Motifs A, C, E, F, the G-loop, and the priming loop are colored in orange, yellow, gray, magenta, cyan, and purple, respectively. N-ter and C-ter indicate the termini of the RdRp domain. RdRps of RNA viruses probably arose from a common ancestor. The RdRp, in association with other proteins required for viral genome synthesis is often called the replicase complex.

The biochemical requirements for genome synthesis may or may not be identical to those required for synthesis of mRNAs. If the two processes differ, the term transcription complex is sometimes used to describe the particular set of proteins required for viral mRNA synthesis.

Upon penetration into the host cell, ribosomes assemble on the genome to synthesize viral proteins. During the replication cycle of positive-strand RNA viruses, among the first proteins to be synthesized are those needed to synthesize additional genomes and mRNAs. A functional definition of a positive-strand virus is that purified or chemically synthesized genomes are infectious Fig. Schematic representation of replication of positive-strand RNA virus genomes. The genome of a positive-strand RNA virus is an mRNA that is translated, upon entry into the cells, to produce proteins needed for transcription and genome replication for example, RdRp.

After initial rounds of translation, the genome serves as the template for synthesis of copy RNA. RdRp is a nonstructural protein, meaning that it is not found within the assembled virion. Instead it is translated directly from the infecting genome shortly after penetration. RdRp and other viral proteins needed for viral RNA synthesis are encoded as a polyprotein that is cleaved by virally encoded proteases. In the case of the picornaviruses and the flaviviruses, all viral proteins structural and nonstructural are synthesized as part of a single long polyprotein.

Other positive-strand RNA viruses i. For each of these groups of viruses, the first synthetic event after genome penetration is transcription Fig.

This is accomplished by viral proteins including viral RdRp that enter cell with the genome. They associate with the genome through interactions with RNA-binding nucleocapsid N or capsid proteins.

Therefore, naked purified away from protein genomic RNA is not infectious, cannot be translated, and will eventually be degraded if transcription is blocked. Before genome replication can proceed, viral mRNAs must be transcribed and translated. If purified virions are gently lysed under appropriate buffer conditions, with the addition of NTPs, mRNAs will be transcribed in the test tube. However, genome RNA will not be synthesized under these conditions Table Schematic representation of replication of genomes of minus-strand RNA viruses.

Upon entry into the cell, the active transcription complex synthesizes mRNAs. This process can also occur in a test tube see Fig. Translation of mRNAs produces proteins required for genome replication. Thus if protein synthesis is blocked in the infected cell, mRNAs continue to by synthesized but genome replication does not occur. Newly synthesized proteins provide the switch from transcription to genome replication.

The genomes of viruses in the order Mononegavirales are unsegmented, negative-strand RNA. Note that genome synthesis does not occur under these conditions. Nonetheless, oncogenes clearly have a deleterious effect on some individuals within the species i.

One particularly striking example occurs in a polycythemia strain of mice carrying the Friend murine leukemia virus. All the mice of this particular strain have polycythemia, a condition characterized by a sustained increase in the number of circulating red blood cells.

It seems that the resident virus codes for a nonfunctional Env viral envelope gene. The protein coded by the degenerate Env gene serves as a mimic for the normal erythropoietin gene of the mouse, causing an increase in red cell production i. Participating in eukaryotic evolution, and accounting in no small way for the generation of new species and new strains of species, as viruses certainly do, are itself a biological function, and another indicator of viral life.

Are viruses living organisms, or are they simply sequences of nucleic acid that have the wherewithal to move from cell to cell. Much of the debate focuses around the definition of life [1] , [26]. How we define life is somewhat arbitrary, and we can certainly produce a definition of life that includes the viruses, if that is what we choose.

There's no urgency to the matter. Once our robots become self-replicating, we'll need to address the definition of life anew. When that time comes, perhaps robots will take the lead and create a definition for life that includes organic viruses and software viruses.

For a moment, let's put our tongues in our cheeks and pretend that we are viruses [8]. As viruses, what would we think of humans and other eukaryotic organisms? Would we be willing to accept humans as fellow living organisms, or would we point to the following list of disqualifiers to conclude that humans just don't make the grade?

In an effort to strengthen their species' gene pool, humans undergo a strange mating process in which the chromosomes of both parents are hopelessly jumbled together to produce an offspring that is unique, and unlike either the father or the mother.

In doing so, humans miss out on the replicative process, performed with the greatest enthusiasm by every virus. Self-replication is one of the fundamental features of life. Because humans cannot replicate themselves, they barely qualify as living organisms. At least, this is what the viruses think. Humans have created a variety of weapons that are fully capable of wiping out all of human life. Viruses generally respect one another's right to co-exist.

In point of fact, if there were no viruses, there would be no DNA replication, no adaptive immune system, no placentas, and no humans [27]. We also see that viral species acquire genes from their hosts, and that viruses retain these genes as they evolve. Presumably, the acquisition of host genes confers some survival advantage upon the virus. Nonetheless, viruses are a self-sufficient class of organism, and no specific instance comes to mind wherein a viral species depended on a human gene for its survival.

Nobody really knows much about the earliest forms of life, and there is plenty of room for conjecture. It's quite feasible that the earliest genetic material consisted of sequences of RNA, and that these RNA molecules moved between the earliest forms of cells. If this were the case, then the earliest genomes were essentially RNA viruses, and this would place humans as direct, but distant descendants of viruses.

There is a current theory, among many competing theories, that the first eukaryotic nucleus was a giant virus that was not totally successful in transforming its proto-eukaryotic host into a virocell [8] , [28] , [29]. We are taught to think of viruses as fragments of nucleic acids wrapped by a capsid i. To a virus, extracellular existence must be akin to a state of suspended animation. Virions come back to life when they invade a eukaryotic cell and create a virocell; a living organism consisting of the hijacked eukaryotic cell whose nuclear machinery is redirected to synthesize viral progeny.

If every eukaryotic cell is conceptualized as a potential virocell, then every eukaryotic species is a potential slave owned by the viral kingdom. The viruses probably think they're doing us a favor. Frankly, most of the cells in a metazoan body lead a vegetative existence, doomed to a fully differentiated, postmitotic, and short existence. Viruses re-animate postmitotic cells, and create a thriving center for viral life from a lackluster population of eukaryotic cells, as virocells. If we accept that viruses are living organisms, on equal footing with bacteria, achaeans, and eukaryotes, then we must accept the challenge of creating a classification of viruses based on phylogeny descent from evolving ancestral species , and abandon viral groupings based solely on phenetics i.

There is a problem with the notion of a purely phylogenetic classification of viruses; it may be impossible [ Glossary Phenetics ]. Let's take a look at a few of the impediments to establishing a viral phylogeny that is comprehensive, testable, and credible. Simply put, the greater the number of species, the more work is required to prepare a taxonomy. Every new species requires a certain irreducible amount of study, and if new species are being discovered at a rate that exceeds our ability to describe and classify known species, then the list of unassigned species will become infinitely long over time.

The classification of cellular organisms is built on the premise that each of the major classes i. In the case of viruses, we really have no way of describing the ancestor of all extant viruses, and we do not have a strong reason to assume that all the viruses we see today came from any single class of viruses.

Furthermore, we define viruses as being obligatory parasites, requiring one of the major classes of cellular organisms for a host. If this were the case, then viruses, as we have come to define them, could not have existed prior to the existence of host organisms to parasitize. Hence, if viruses existed prior to the emergence of cellular life, then the root of the viruses was not a virus, insofar as they could not have parasitized cellular hosts.

If the root of the viruses was not a virus, then it may have been almost anything, and we could not rule out the existence of multiple root organisms, accounting for the widely varying versions of viral genomes that we observe today.

Games of phylogenetic logic are harmless fun, but they illustrate how it is impossible to create a top-down classification of viruses, if we know nothing about the biological features that would define the top class. For the most part, viruses do not repair their genomes. A notable exception is the megavirus Cafeteria roenbergensis [30]. Presumably, we will find that other megaviruses have DNA repair pathways, but the small, simple viruses have rates of mutation in DNA and RNA, with no mechanism to repair the damage.

This means that genome-damaged viruses have two choices: to die or to live with, and replicate, their mutations. Consequently, viral genomes tend to degenerate quickly, producing lots of variants.

Species mutability is particularly prevalent among the RNA viruses e. Mutational variations of a virus seldom produce a new species. Instead, variations produce diversity in the viral gene pool of the species.

If new mutations do not produce an alteration in the specificity of host organisms, or in the construction of the virocell, then the variant viral replicants resulting from mutations will usually preserve their membership in the same viral species [Glossary Virocell ]. Still, all those viral genomic variants complicate the job of the viral taxonomist. Basically, the high rate of mutation in viruses yields lots of genomic variation among viral populations, making it easy for bioinformaticians to detect species diversity where none exists.

We can easily imagine a situation wherein new species are discovered, and old species are declared extinct, because we simply do not have the time and manpower to carefully examine every genomic variant for the structural and physiologic features that determine its correct taxonomic classification. Bioinformaticians off-handedly refer to the variant genomes, resulting from mutations and replication errors, as quasispecies [31].

Viral reassortment is a process wherein whole segments the equivalent of viral chromosomes are exchanged between two viruses infecting the same cell. Viral reassortment has been observed in four classes of segmental RNA viruses: Bunyaviridae, Orthomyxoviridae, Arenaviridae, and Reoviridae. Following reassortment, a new species of virus may appear, and this new species will contain segments of two parental species. This poses a serious problem for traditional taxonomists, who labor under the assumption that each new species has one and only one parental species [32].

It is the uniparental ancestry of biological classifications that accounts for their simplicity, and for the concept of lineage, wherein the ancestry of any species can be computed from an uninterrupted line of classes stretching from the species level to the root level.

When a species has more than one parent, then its lineage is replaced by an inverted tree. The tree branches outwards with each class reaching to more than one parent class, iteratively, producing a highly complex ancestry wherein the individual classes have mixed heritage.

Bioinformaticians have no problem creating multiparental classifications, and have used them to organize and model for biological processes e. They call such constructs ontologies, and have an assortment of computational tools to construct, deconstruct, and analyze complex representations of class relationships. The pros and cons of single-parent class relationships versus multiparent class relationships have been argued at great length in the bioinformatics literature and cannot be fully explored here [34] , [35].

Suffice it to say that no matter how many species we must accommodate, a simple classification will always provide an ordered set of class relationships that can be fully absorbed by the human mind. Ontologies are highly complex, often uncomputable, and chaotic e.

It remains to be seen whether the ontologic model can be usefully applied to viral classifications. A sense of hopefulness is based, in no small part, on observations of the physical world.

Despite our sense that anything is possible in the vastness of space, we see an awful lot of sameness throughout the universe.

Wherever we aim our telescopes, we see galaxies, most of which are flat and spiral, often having about the same size, and composed of the same objects: stars, planets, gas, dust, and black holes. A small set of physical laws impose stability everywhere at once, and the result is the somewhat repetitious universe in which we live.

Likewise, despite the large number of species living on our planet, they are all variations of a few common themes that can be encapsulated under a simple classification.

About a half billion years ago, the early metazoan classes i. This period, which lasted about 40 million years or so, is known as the Cambrian Explosion. The same body plans that evolved during the Cambrian explosion account for nearly all of the classes of animals that live today.

This is to say that since the Cambrian, no new body plans have gained entry into the metazoan world. Much has been written about the Cambrian explosion, much of it focused on why metazoan body plans are so few, and why the world lacks newly evolved entries [36].

We have observed as a general rule of biology, that no matter how easy it may be for a class of organisms to speciate, there always seems to be a limited number of general classes into which all the species can be assigned. It is as though the evolutionary process itself confines classes to a smaller and smaller repertoire of available designs. When we think that we have encountered a class of life that is too complex for simple classification, we are usually proven wrong.

For example, in the first two-thirds of the 20th century, the classification of bacteria was considered a hopeless task, insofar as bacteria of different classes were known to exchange DNA among themselves, in a general process known as horizontal gene transfer.

If bacteria were constantly exchanging genetic material, then it seemed that every bacteria was an amalgam of other bacteria and could not be sensibly classified. Be that as it may, bacteria were found to have a convincing phylogenetic order, based on the ancestral lineage of highly conserved species of rRNA that distinguished the bacteria from archaeal bacteria and further distinguished the classes and subclasses of bacteria [37] , [38].

In the case of viruses that mutate at a high rate, that exchange large pieces of their DNA, that extract DNA from their host organisms, and that produce an uncountably large number of diverse species, one might think that a classification would be an impossible task.

Not so. Instead, we are finding fundamental molecular motifs that can be used to classify viruses into biological groups that share phylogenetic origins [39] , [16]. For example, despite the sequence variations that occur in rapidly mutating viruses, scientists are finding that the three-dimensional folds of protein molecules are conserved, and that viruses can be grouped into the so-called fold families, which can in turn be grouped into fold super families, that preserve phylogenetic relationships among viral lineages [39].

We shouldn't be surprised that viruses, like every other class of organism, falls into a rather limited set of phylogenetic classes. Because all viruses are parasitic, we can see why all viral species are constrained to evolve in a manner that maintains their host compatibility [17]. A demonstration of host-specific constraints on viruses is found by examining the specificity of viruses for the highest classes of organisms. Virus infections are found in Class Archaea, Class Bacteria, and Class Eukaryota, but there is no instance in which any single class of viruses is capable of infecting more than one of these classes of cellular organisms.

Furthermore, within a class of cellular organisms, there are only rare instances of classes of virus that can infect distantly related subclasses. For example, there are virtually no viruses that can infect both Class Animalia and Class Plantae rare exceptions are claimed [40]. Furthermore, as the host evolves, so must the virus. Hence, we might expect to find ancestral lineages of viruses that shadow the lineage of their host organisms.

The relatively recent discovery of NCLDVs nucleocytoplasmic large DNA viruses, popularly known as giant viruses has greatly expanded our notion of viral existence [45] , [46].

The NCLDVs, with their large genomes and complex sets of genes, have provided taxonomists with an opportunity to establish ancestral lineages among some of these viruses [45] , [46].

At this time, the classification of viruses is somewhat crude. Anything you choose as a classifying principle fails to biologically unify the subclasses. For example, if you classify viruses by their genomic molecules i. When we list viruses based on method of contagion, by persistence within host i. Though we cannot as yet classify viruses strictly by their evolutionary lineage, we can usefully group viruses based on the physical characteristics of their genomes.

The Baltimore Classification divides viruses into seven groups based on whether their genome is DNA, RNA, single stranded, or double stranded, the sense of the single strand, and the presence or absence of a reverse transcriptase. Here are the classes of the pathogenic viruses. This classification, though nonphylogenetic in concept, has the great advantage of being comprehensive: every known virus can be assigned to a group within the Baltimore Classification.

It is worth repeating that when we use the Baltimore Classification or any alternate viral classification, for that matter we must grudgingly accept the fact that biologically relevant features of grouped viruses will cross taxonomic boundaries. Consider the arboviruses. Arbovirus is a shortened name for Arthropod borne virus. The arboviruses fall into several different groups of viruses.

The principle vectors of the arboviruses are mosquitoes, ticks. Over arboviruses, infecting a variety of animals, have been described [47]. The arboviruses, organized by their transmission vectors, as shown below, cross multiple viral groups. It would seem that we do not know enough about the origin and phylogeny of the different classes of viruses to create a true classification, wherein viruses of a class share a common set of inherited relationships.

There is, however, hope for a future in which viruses can be organized by phylogenetic principles. Highly innovative work in the field of viral phylogeny is proceeding, from a variety of different approaches, including: inferring retroviral phylogeny by sequence divergences of nucleic acids and proteins in related viral species [16] ; tracing the acquisition of genes in DNA viruses [41] ; and dating viruses by the appearance of viral-specific antibodies in ancient host cells [12].

Because viruses evolve very rapidly, it is possible to trace the evolution of some viruses, with precision, over intervals as short as centuries or even decades [39] , [42] , [43] , [44]. It should be noted that before the advent of ribosomal sequence analysis, and as recently as the early s, bacterial phylogeny was considered a hopeless field [37].

Bacteria were grouped by morphology, nutritional requirements, and enzymatic reactions e. The field of viral phylogeny is quickly catching up with the phylogeny of living organisms. Aside from this property, these viruses vary greatly.

Some species have envelopes; others do not. Some species have circular genomes; others have linear genomes. The size of the viral genome can vary as much as fold among different species of the group. The host range covers the range of living organisms. Bacteria, archaeans, eukaryotes are infected by one or the other Group I viruses.

The group has been subclassed based on shared morphologic properties, six of these subclasses contain human pathogens: Adenoviridae, Herpesviridae, Poxviridae, Papillomaviridae, Polyomaviridae, and Mimiviridae. Most of the DNA transforming viruses i. Unlike the retroviruses Group VI , which contain genes that are homologous with cancer-causing oncogenes, the DNA transforming viruses do not contain oncogenes. The Group I DNA transforming viruses seem to cause cancer through a mechanism related to their ability to induce replication in their host cells [Glossary Hepatitis viruses ].

Members of Class Herpesviridae are commonly known as herpesviruses. These viruses produce acute disease characterized by lytic i. After cells are infected by virus particles, the viral genome migrates to the host nucleus, where replication and transcription of the viral genes occurs.

After a latent phase, viruses may precipitate a lytic phase, manifesting as clinical disease. The recurring disease may be clinically distinct from the initial infection e. Some of the herpesviruses are DNA transforming viruses. The human herpesviruses are: Epstein-Barr virus, Herpes simplex viruses, Varicella virus, and Human herpesviruses 6, 7, and 8, and Cytomegalovirus. Epstein-Barr virus infects almost all adults. Its persistence makes it one of the most prevalent human pathogens.

It manifests acutely as mononucleosis, a pharyngitis accompanied by lymphocytosis increases lymphocytes in the peripheral blood with morphologic alterations in infected lymphocytes. Splenomegaly and hepatomegaly may occur. The generalized symptoms of the disease, particularly fatigue, may extend for months or longer, and some cases of mononucleosis recur. Epstein-Barr virus is a DNA transforming virus and accounts for several cancers, including Hodgkin lymphoma, Burkitt lymphoma, nasopharyngeal carcinoma, and central nervous system lymphoma.

A role for the virus in several autoimmune diseases has been suggested. Herpes simplex type 1 causes cold sores, and Herpes simplex types 2 causes genital herpes.

Both diseases may recur after initial infection. As mentioned, Herpes virus varicella-zoster causes chickenpox on first infection and herpes zoster, also known as shingles, on reactivation.

Herpesvirus simiae, also known as B virus, infects macaque monkeys, without causing severe disease. In rare circumstances, humans may become infected with this virus, from the monkey reservoir. Human infection typically results in a severe encephalopathy. Human herpesvirus type 6 HHV6 and type 7 HHV7 produce exanthem subitum, also known as roseola infantum and as sixth disease.

Readers should not confuse sixth disease with fifth disease. Fifth disease, also known as erythema infectiosum and slapped face disease, is caused by Parvovirus B These diseases take their names from an historical diagnostic dilemma faced by pediatricians, who regularly encountered six clinical syndromes of childhood rashes.

Four of the childhood rashes had known etiologies. Human herpesvirus type 8 HHV8 is a DNA transforming virus that can cause Kaposi sarcoma, primary effusion lymphoma, and some forms of Castleman disease.

Kaposi sarcoma is a cancer characterized by focal proliferations of small blood vessels, occurring most often in the skin. Immunosuppressed patients e. Interestingly, if immunosuppression is halted, the Kaposi sarcoma may regress [49]. It is presumed that sustained viral replication is necessary for early tumor growth. Cytomegalovirus infects about half of the world population, with most individuals suffering no ill effects. Once infected, the virus usually persists for the life of the individual.

In a minority of cases, particularly among immune-compromised individuals e. The disease is known as cytomegalic inclusion body disease, and, as the name suggests, cytoplasmic and nuclear inclusion bodies characterize actively infected cells. When the virus is transmitted transplacentally, by mothers infected during their pregnancy, the newborn may suffer developmental damage to the brain and other organs Fig. Cytomegalovirus infection of the lung.

Near the top, center of the image is an infected pneumocyte with a highly enlarged nucleus. The bulk of the nucleus is occupied by a dense inclusion, sometimes called Cowdry body, containing viral nucleocapsids.

Surrounding the inclusion is a clear zone. Such nuclear inclusions, observed with all species of herpes viruses that infect humans, have long served as an important clue to the diagnosis and the pathogenesis of viral diseases.

Class Adenoviridae contains the human adenoviruses of which there are 57 types, with different clinical syndromes associated with specific subtypes of the virus. Most adenoviral diseases present clinically as respiratory illness, conjunctivitis i.

Infections may present clinically as tonsillitis simulating strep throat , pharyngitis croup , otitis media, pneumonia, meningoencephalitis, and hemorrhagic cystitis. Adenoviruses are commonly spread by aerosolized droplets, and are particularly stable in the external environment. Human papillomaviruses cause skin warts, laryngeal warts, and genital warts.

Warts are benign tumors composed of proliferating squamous cells. In some cases, these human papillomavirus-induced warts progress to become invasive squamous cell carcinomas Fig. The clump of flat epithelial cells on the left is normal squamous cells that line the uterine cervix. The clump of three cells on the right is squamous epithelial cells demonstrating koilocytosis, a cytopathic effect produced by human papillomavirus infection.

Notice that the nuclei are enlarged, appearing approximately times as large as normal nuclei on left. Surrounding each nucleus right clump is an abnormal zone of pale cytoplasm, typical of koilocytosis. Beyond the pale zone is a thinner zone of normal-appearing cytoplasm extending out to the cell membrane. Class Polyomaviridae contains several viruses that infect humans: BK polyomavirus, JC polyomavirus, and Simian virus The BK polyomavirus rarely causes disease in infected patients, and the majority of humans carry the latent virus.

Latency can shift to lytic infection after immunosuppression, producing a clinical nephropathy. The JC polyomavirus persistently infects the majority of humans, but it is not associated with disease in otherwise healthy individuals.

Rarely, in immune-compromised patients, JC polyomavirus may produce progressive multifocal leukoencephalopathy. The virus targets myelin-producing oligodendrocytes in the brain to produce areas of demyelination and necrosis. Simian virus 40 SV40 infects monkeys and humans, but there is no evidence at this time confirming a role in human disease.

Members of Class Orthopoxvirus produce disease characterized by pustules of the skin, and lymphadenopathy. The smallpox virus is remarkable for its extremely narrow host range: humans only. The virus infects the skin and the mucosa of the upper respiratory tract, where it produces a pustular, weeping, and rash. In the respiratory mucosa, the rash interferes with breathing. If the disease becomes hemorrhagic, the prognosis worsens. Smallpox is reputed to have killed about million people in the 20th century, prior to the widespread availability of an effective vaccine.

Smallpox has been referred to as the greatest killer in human history. No doubt, death rates climbed because the disease was easily communicable via aerosols, fomites, bodily fluids, or direct contact with patients with rash. Aside from the remarkable success of vaccination, eradication was no doubt made possible because smallpox has no animal reservoir. At this time, vaccination is not routinely performed and is reserved primarily as an antiterror measure, for personnel entering a zone where there is a bioweapons threat.

Variola minor is a virus closely related to Variola major that produces a milder disease. These diseases are known by various names including alastrim, cottonpox, milkpox, whitepox, and Cuban itch. Infection with Variola minor is thought to produce cross-resistance to Variola Major and vice versa. Vaccinia virus is the laboratory-grown poxvirus, of obscure heritage, that does not precisely correspond to known viruses that reside outside the laboratory or clinic i.

Vaccinations with vaccinia virus have been known to produce, in rare cases, a variety of clinical disorders, ranging from vaccinia localized pustular eruptions to generalized vaccinia, to progressive vaccinia, to vaccinia gangrenosum, and to vaccinia necrosum. Other conditions associated with vaccinations include eczema vaccinatum and postvaccinial encephalitis. Smallpox vaccination, aside from eradicating mankind's greatest killer, may have heretofore unrecognized public health value.

The number of currently known pathogenic organisms, their variant subtypes, their ability to mutate, and the emergence of newly encountered pathogens make it impossible to develop vaccines for every organism that infects humans. Consequently, vaccine experts are searching for vaccines that confer immunity, partial or full, for several different pathogens or for several variants of a single pathogen [50].

An interesting development in this field is that the smallpox vaccine may confer limited protection against HIV human immunodeficiency virus infection.

Both viruses enhance their infectivity by exploiting a receptor, CCR5, on the surface of white blood cells. This shared mode of infection may contribute to the cross-protection against HIV that seems to come from smallpox vaccine. It has been suggested that the emergence of HIV in the s may have resulted, in part, from the cessation of smallpox vaccinations in the late s [51].

Buffalopox, cowpox, and monkeypox produce diseases in animal reservoirs and rarely infect humans. Human infections occur from close contact with infected animals and manifest much like smallpox, but milder. Members of Class Parapoxvirus infect vertebrates, particularly sheep, goats, cattle, and red squirrels. Humans, though rarely infected, may develop painful hand sores. A similar condition can occur in humans who handle the udders of cows infected with Milker's nodule virus.

Class Molluscipoxvirus contains one species infectious in humans, Molluscum contagiosum virus. Molluscum contagiosum is an eruption of wart-like skin lesions that are easily diagnosed on histological examination by their distinctive cellular inclusions so-called molluscum bodies.

There are no known animal reservoirs. Infection is spread from human to human. Treatment is not always necessary, as individual lesions will regress within two months. However, auto-inoculation of the virus may produce new skin lesions, thus prolonging the disease. Members of Class Yatapoxvirus infect primates in equatorial Africa.

Infections can spread to humans by insect vectors. Tana poxvirus produces a pock-forming skin infection, with fever and lymphadenopathy in infected humans i. The Yaba monkey tumor virus produces histiocytomas in monkeys. Histiocytomas are proliferative lesions of fibrous tissue that yield tumor-like nodules. These virally induced histiocytomas in monkeys grow rapidly following infection, and then regress over the ensuing month [52].

Yaba monkey tumor virus and Yaba-like disease virus, like all members of Class Yatapoxvirus, are considered potential human pathogens. Class Mimiviridae, discovered in , occupies a niche that seems to span the biological gulf separating living organisms from viruses.

Members of Class Mimiviridae are complex, larger than some bacteria, with enormous genomes by viral standards , exceeding a million base pairs and encoding upwards of proteins. The large size and complexity of Class Mimiviridae exemplifies the advantage of a double-stranded DNA genome. DNA is much more chemically stable than RNA, and can be faithfully replicated, even when its length exceeds a billion base pairs. Class Megaviridae is a newly reported October class of viruses, related to Class Mimiviridae, but larger [45].

As previously noted, the life of a mimivirus is not very different from that of obligate intracellular bacteria e. Acanthamoeba polyphaga mimivirus is a possible human pathogen. Some patients with pneumonia have been shown to have antibodies against the virus [53]. Though Myxoma virus is not a human pathogen, it seems appropriate to include some mention of this member of Class Poxviridae, due to the role humans have played in its history.

Retroviruses can be used as vectors to deliver new genes to animal cells. However, they do not produce viruses. Why not? There are no LTRs. There is no reverse transcriptase. Reverse transcriptase is present but not needed. There is no RNA polymerase. RNA polymerase is present. No, amino acids are present.

No, both are present. LTRs have several functions. They not only help integrate the viral genome into the DNA of an infected cell, they also indicate where RNA transcription begins and ends. Without RNA, there is no virus. The next step in turning a retrovirus into a vector with a new gene is to transform the producer cells with a plasmid that contains the new gene.

Once transformed with the plasmid, these cells produce modified virus. What sequences does the virus now carry on its genome?

That is incorrect. RNA genome contains gag, pol, and env. No, retroviruses carry RNA. DNA genome contains gag, pol, and env.