Jump to content

Remedy/Viruses

Add links
From Wikiversity
This negative stained transmission electron micrograph (TEM) depicts a number of filamentous Marburg virions. Credit: CDC/ Dr. Erskine Palmer, Russell Regnery, Ph.D.{{free media}}

This negative stained transmission electron micrograph (TEM) depicts a number of filamentous Marburg virions, which had been cultured on Vero cell cultures, and purified on sucrose, rate-zonal gradients. Note the virus’s morphologic appearance with its characteristic “Shepherd’s Crook” shape; Magnified approximately 100,000x. Marburg hemorrhagic fever is a rare, severe type of hemorrhagic fever which affects both humans and non-human primates. Caused by a genetically unique zoonotic (that is, animal-borne) RNA virus of the filovirus family, its recognition led to the creation of this virus family. The four species of Ebola virus are the only other known members of the filovirus family. Marburg virus was first recognized in 1967, when outbreaks of hemorrhagic fever occurred simultaneously in laboratories in Marburg and Frankfurt, Germany and in Belgrade, Yugoslavia (now Serbia).

Def. a "submicroscopic, non-cellular structure consisting of a"[1] "core of DNA or RNA surrounded by a protein coat that requires a living [host][2] cell to reproduce [replicate][3] [ and][4] often causes disease in the host organism"[5]; such agents are often classed as nonliving infectious particles and less often as microorganisms"[6] is called a virus.

Viruses

[edit | edit source]

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism.[7] Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea.[8][9] Since an 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus in 1898,[10] more than 9,000 virus species have been described in detail[11] of the millions of types of viruses in the environment.[12] Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity.[13][14]

Infectious doses

[edit | edit source]

The infectious dose of norovirus required to produce infection in humans is less than 100 particles.[15]

The variety of host cells that a virus can infect is called its "host range", which can be narrow, meaning a virus is capable of infecting few species, or broad, meaning it is capable of infecting many.[16]

Bacteriophages

[edit | edit source]

A group of viruses that infect bacteria, now called bacteriophages was discovered.[16] (or commonly 'phages'). Viruses that, when added to bacteria on an agar plate, would produce areas of dead bacteria. He accurately diluted a suspension of these viruses and discovered that the highest dilutions (lowest virus concentrations), rather than killing all the bacteria, formed discrete areas of dead organisms. Counting these areas and multiplying by the dilution factor allowed him to calculate the number of viruses in the original suspension.[17]

Adenoviridae

[edit | edit source]
Transmission electron micrograph shows two adenovirus particles. Credit: GrahamColm.{{free media}}
The diagram shows the structure of an adenovirus. 1 = penton capsomers, 2 = hexon capsomers, and 3= viral genome (linear dsDNA). Credit: Pico en el Ojo.{{free media}}

Adenoviruses (members of the family Adenoviridae) are medium-sized (90–100 nm), nonenveloped (without an outer lipid bilayer) viruses with an icosahedral nucleocapsid containing a double-stranded DNA genome.[18] Their name derives from their initial isolation from human adenoids in 1953.[19]

They have a broad range of vertebrate hosts; in humans, more than 50 distinct adenoviral serotypes have been found to cause a wide range of adenovirus infection (illnesses), from mild respiratory infections in young children (known as the common cold) to life-threatening multi-organ disease in people with an immunodeficiency (weakened immune system).[18]

This family contains the following genera:[20]

  • Atadenovirus
  • Aviadenovirus
  • Ichtadenovirus
  • Mastadenovirus (including all human adenoviruses)
  • Siadenovirus
  • Testadenovirus

In humans, currently there are 88 human adenoviruses (HAdV serotypes) in seven species (Human adenovirus A to G):[21]

  • Human adenovirus A: 12, 18, 31
  • Human adenovirus B: 3, 7, 11, 14, 16, 21, 34, 35, 50, 55
  • Human adenovirus C: 1, 2, 5, 6, 57[22]
  • Human adenovirus D: 8, 9, 10, 13, 15, 17, 19, 20, 22, 23, 24, 25, 26, 27, 28, 29, 30, 32, 33, 36, 37, 38, 39, 42, 43, 44, 45, 46, 47, 48, 49, 51, 53, 54, 56,[23] 58, 59, 60, 62, 63,[24] 64, 65, 67, 69,[25] 70, 71, 72, 73, 74, 75
  • Human adenovirus E: 4
  • Human adenovirus F: 40, 41
  • Human adenovirus G: 52[26]

Different types/serotypes are associated with different conditions:[27]

  • respiratory disease (mainly species HAdV-B and C)
  • conjunctivitis (HAdV-B and D)
  • gastroenteritis (HAdV-F types 40, 41, HAdV-G type 52)
  • obesity or adipogenesis (HAdV-A type 31, HAdV-C type 5, HAdV-D types 9, 36, 37)[28]

All these types are called Human mastadenovirus A–G by the International Committee on Taxonomy of Viruses (ICTV), because all are members of the genus Mastadenovirus.

The penton bases are associated with protruding fibers that aid in attachment to the host cell via the receptor on its surface.[29]

The structure of the human adenovirus was solved at the atomic level, making it the largest high-resolution model ever, composed of around 1 million amino acid residues and around 150 MDa.[30][31][32]

Orthopoxvirus phylogeny
nucleocapsid envelope genome By sequence By gene content Genus species Common name
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human A human adenovirus A
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human B human adenovirus B
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human C human adenovirus C
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human D human adenovirus D
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human E human adenovirus E
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human F human adenovirus F
icosahedral nonenveloped double-stranded DNA genome Adenovirus virus between 26 and 48 Kbp.[18] 22 to 40 genes Mastadenovirus human G human adenovirus G

Asfarviridae

[edit | edit source]
Electron micrograph shows a African swine fever virus particle. Credit: .{{free media}}

African swine fever virus (ASFV') is a large, double-stranded DNA virus in the Asfarviridae family,[33] the causative agent of African swine fever (ASF), causes a hemorrhagic fever with high mortality rates in domestic pigs; some isolates can cause death of animals as quickly as a week after infection, persistently infects its natural hosts, warthogs, bushpigs, and soft ticks of the genus Ornithodoros, which likely act as a vector, with no disease signs.[34] It does not cause disease in humans.[35][36] ASFV is endemic to sub-Saharan Africa and exists in the wild through a cycle of infection between ticks and wild pigs, bushpigs, and warthogs. The disease was first described after European settlers brought pigs into areas endemic with ASFV, and as such, is an example of an emerging infectious disease.

ASFV replicates in the cytoplasm of infected cells.[33] It is the only virus with a double-stranded DNA genome known to be transmitted by arthropods.[37]

Coronaviridae

[edit | edit source]
Coronaviruses are a group of viruses that have a halo, or crown-like (corona) appearance when viewed under an electron microscope. Credit: CDC/Dr. Fred Murphy.{{free media}}

Coronaviruses constitute the subfamily Orthocoronavirinae, in the family Coronaviridae, order Nidovirales and realm Riboviria.[38][39] They are enveloped viruses with a positive-sense single-stranded RNA genome and a nucleocapsid of helical symmetry.[40] The genome size of coronaviruses ranges from approximately 26 to 32 kilobases, one of the largest among RNA viruses.[41]

"Coronaviruses possess the largest genomes [26.4 kb (ThCoV HKU12) to 31.7 kb (SW1)] among all known RNA viruses [...] [2,13,16]."[41] They have characteristic club-shaped peplomer (spikes) that project from their surface, which in electron micrographs create an image reminiscent of the solar corona, from which their name derives.[42] "[T]here is also a characteristic "fringe" of projections 200 A long, which are rounded or petal shaped ... This appearance, recalling the solar corona, is shared by mouse hepatitis virus and several viruses recently recovered from man, namely strain B814, 229E and several others."[42]

Coronavirus phylogeny
nucleocapsid envelope genome sense By sequence By gene content Genus species Common name
helical symmetry enveloped single-stranded RNA positive OC43
Alphacoronavirus human coronavirus 229E Human coronavirus 229E

Genome organisation of SARS-CoV. Nsp3 and full-length SUD with subdomains N, M, and C are highlighted. Mpro, main (or 3CL) protease; ssRBP, single-stranded RNA-binding protein; RdRp, RNA-dependent RNA polymerase; ExoN, exonuclease; NendoU, uridine-specific endoribonuclease; MT, methyltransferase; Spike, spike protein; E, envelope protein; M, membrane (matrix) protein; N, nucleocapsid protein; Ac, acidic domain; X, X-domain; SUD, SARS-unique domain; PL2pro, papain-like protease; TM, transmembrane region; Y, Y-domain.

Herpesviridae

[edit | edit source]
Electron micrograph shows a Human alphaherpesvirus 3 virion. Credit: CDC/Dr. Erskine Palmer/B.G. Partin.{{free media}}

Human herpesvirus 3 (HHV-3)[43]

Varicella-zoster virus[44]

Human alphaherpesvirus 3 (HHV-3), usually referred to as the varicella-zoster virus (VZV), is one of nine herpesviruses known to infect humans. It causes chickenpox, a disease most commonly affecting children, teens, and young adults, and shingles in adults; shingles is rare in children. VZV infections are species-specific to humans, but can survive in external environments for a few hours.[45]

Many years after the person has recovered from chickenpox, VZV can reactivate to cause neurological conditions.[46]

Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal nerve and dorsal root ganglia.[47]

Lesions most commonly occur on the face, throat, the lower back, the chest and shoulders.[48]

In about a third of cases,[49] VZV reactivates later in life, producing a disease known as shingles or herpes zoster.

The individual lifetime risk of developing herpes zoster is thought to be between 20% and 30%, or approximately 1 in 4 people; however, for individuals aged 85 and over, this risk increases to 1 in 2 people.[50]

In a study from Sweden the annual incidence of herpes zoster infection is estimated at a total of 315 cases per 100,000 inhabitants for all ages and 577 cases per 100,000 for people 50 years of age or older.[51]

VZV can also infect the central nervous system, with an article reporting an incidence rate of 1.02 cases per 100,000 inhabitants in Switzerland, and an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden.[52]

Serious complications of varicella zoster infection include Mollaret's meningitis, zoster multiplex, and inflammation of arteries in the brain leading to stroke,[53]

Reye’s syndrome mostly affects children and teenagers, using aspirin during infection can increase this risk.[48]

The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each approximately 8 nm long.[54]

The genome was first sequenced in 1986.[55] It is a linear duplex DNA molecule, a laboratory strain has 124,884 base pairs. The genome has 2 predominant isomers, depending on the orientation of the S segment, P (prototype) and IS (inverted S) which are present with equal frequency for a total frequency of 90–95%. The L segment can also be inverted resulting in a total of four linear isomers (IL and ILS). This is distinct from HSV's equiprobable distribution, and the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes, about which little is known. (It is known that HSV circularizes on infection.) There are at least 70 open reading frames in the genome.

There are at least five clades of this virus.[56] Clades 1 and 3 include European/North American strains; clade 2 are Asian strains, especially from Japan; and clade 5 appears to be based in India. Clade 4 includes some strains from Europe but its geographic origins need further clarification. There are also four genotypes that do not fit into these clades.[57]

Phylogenetic analysis of VZV genomic sequences resolves wild-type strains into 9 genotypes (E1, E2, J, M1, M2, M3, M4, VIII and IX).[58][59]

Sequence analysis of 342 clinical varicella and zoster specimens from 18 European countries identified the following distribution of VZV genotypes: E1, 221 (65%); E2, 87 (25%); M1, 20 (6%); M2, 3 (1%); M4, 11 (3%). No M3 or J strains were observed.[58] Of 165 clinical varicella and zoster isolates from Australia and New Zealand typed using this approach, 67 of 127 eastern Australian isolates were E1, 30 were E2, 16 were J, 10 were M1, and 4 were M2; 25 of 38 New Zealand isolates were E1, 8 were E2, and 5 were M1.[60]

The mutation rate for synonymous and nonsynonymous mutation rates among the herpesviruses have been estimated at 1 × 10−7 and 2.7 × 10−8 mutations/site/year, respectively, based on the highly conserved gB gene.[61]

Matonaviridae

[edit | edit source]
Transmission electron micrograph show rubella viruses. Credit: CDC/Dr. Erskine Palmer.{{free media}}

Rubella virus (Rubivirus rubellae) is assigned to the Rubivirus genus.[62]

Rubiviruses is classified as part of the family Matonaviridae distinguishing rubella from measles and scarlet fever.[63]

The genome has 9,762 nucleotides and encodes 2 nonstructural polypeptides (p150 and p90) within its 5′-terminal two-thirds and 3 structural polypeptides (C, E2, and E1) within its 3′-terminal one-third.[64]

There are three sites that are highly conserved in Matonaviruses: a stem-and-loop structure at the 5' end of the genome, a 51-nucleotide conserved sequence near the 5' end of the genome and a 20-nucleotide conserved sequence at the subgenomic RNA start site. Homologous sequences are present in the rubella genome.[64]

The genome encodes several non-coding RNA structures; among them is the rubella virus 3' cis-acting element, which contains multiple stem-loops, one of which has been found to be essential for viral replication.[65]

The genome has the highest G+C content of any currently known single stranded RNA virus (~70%).[66]

While alphavirus virions are spherical and contain an icosahedral nucleocapsid, RuV virions are pleiomorphic and do not contain icosahedral nucleocapsids.[63]

"Phylogenetic analysis of the RNA-dependent RNA polymerase of alphaviruses, rubella virus and other positive-sense RNA viruses shows the two genera within the Togaviridae are not monophyletic. In particular, rubella virus groups more closely with members of the families Benyviridae, Hepeviridae and Alphatetraviridae, along with several unclassified viruses, than it does with members of the family Togaviridae belonging to the genus Alphavirus."[63]

Rubivirus phylogeny
nucleocapsid envelope genome sense By sequence By gene content Genus species Common name
icosahedral enveloped single-stranded RNA positive three sites 9,762 nucleotides Rubivirus rubellae Rubella virus (RuV)

Orthomyxoviridae

[edit | edit source]
Influenza A and influenza B virus genome, mRNA, and virion diagram are shown. Credit: Dan Dou, Rebecca Revol, Henrik Östbye, Hao Wang, and Robert Daniels.{{free media}}

"Influenza A and B viruses. (A) Schematic of the eight viral RNA (vRNA) gene segments that comprise the influenza A and B genomes. The 5′ and 3′ untranslated regions (UTRs), which contain the viral promoters, are represented with a line, and the box corresponds to the coding region within each vRNA. (B) Diagram of the viral mRNAs that are transcribed from the IAV (left) and IBV (right) vRNA templates. Boxes indicate the viral gene product encoded by each mRNA and the dashed lines show the alternative splicing of the IAV M and NS transcripts, as well as the IBV NS transcript. Red circles represent the 5′ M7pppG cap, black lines denote the 10–13 nucleotide, host-derived primers that are obtained by the cap-snatching mechanism of the viral polymerase. A(n) corresponds to the 3′ poly-A tail produced by reiterative stuttering of the viral polymerase. The smaller mRNAs (empty boxes) represent transcripts that encode nonessential accessory proteins found in many strains, whereas those that are less prevalent (PB2-S1, M42, and NS3) are not illustrated (6–11). (C) Diagram of an influenza A or B virus. The viral membrane proteins HA, NA, and M2 are shown, along with the eight viral ribonucleoproteins (vRNPs), and the matrix protein M1 that supports the viral envelope. To highlight the vRNP components, the illustration beneath the virus is not to scale. A single vRNA gene segment is shown wrapped around multiple nucleoprotein (NP) copies with the conserved promoter regions in the 5′ and 3′ UTRs forming a helical hairpin, which is bound by a single heterotrimeric viral RNA-dependent RNA polymerase (PB1, PB2, and PA). (D) Top view of an influenza virus cross-section showing the vRNP “1 + 7” configuration. vRNPs are depicted with black circles as it is not known if the positioning of a particular vRNP is conserved or interchangeable."[67]

Paramyxoviridae

[edit | edit source]
Morbillivirus measles is shown in an electron micrograph. Credit: Cynthia S. Goldsmith/CDC.{{free media}}
Transmission electron microscopy (TEM) micrograph shows a mumps virus particle. Credit: CDC/F. A. Murphy.{{free media}}

Paramyxoviridae is a family of negative-strand RNA viruses in the order Mononegavirales.[68][69] Vertebrates serve as natural hosts.[70] Diseases associated with this family include measles, mumps, and respiratory tract infections.[71] The family has four subfamilies, 17 genera, and 78 species, three genera of which are unassigned to a subfamily.[72]

Morbillivirus measles (MeV), also called measles virus (MV), is a Negative-sense single-stranded RNA virus, enveloped, non-segmented RNA virus of the genus Morbillivirus within the family Paramyxoviridae.

This thin-section transmission electron micrograph (TEM, on the top right) revealed the ultrastructural appearance of a single virus particle, or “virion”, of measles virus. The measles virus is a paramyxovirus, of the genus Morbillivirus. It is 100-200 nm in diameter, with a core of single-stranded RNA, and is closely related to the rinderpest and canine distemper viruses. Two membrane envelope proteins are important in pathogenesis. They are the F (fusion) protein, which is responsible for fusion of virus and host cell membranes, viral penetration, and hemolysis, and the H (hemagglutinin) protein, which is responsible for adsorption of virus to cells. There is only one antigenic type of measles virus. Although studies have documented changes in the H glycoprotein, these changes do not appear to be epidemiologically important (i.e., no change in vaccine efficacy has been observed).

Prior to 1963, almost everyone got measles; it was an expected life event. Each year in the U.S. there were approximately 3 to 4 million cases and an average of 450 deaths, with epidemic cycles every 2 to 3 years. More than half the population had measles by the time they were 6 years old, and 90 % had the disease by the time they were 15. This indicates that many more cases were occurring than were being reported. However, after the vaccine became available, the number of measles cases dropped by 98 % and the epidemic cycles drastically diminished.

Measles virus is rapidly inactivated by heat, light, acidic pH, ether, and trypsin. It has a short survival time (<2 hours) in the air, or on objects and surfaces.

This 1976 negative stained transmission electron micrograph (TEM, second down on the right) depicted the ultrastructural features displayed by the mumps virus (Orthorubulavirus mumps, synonym Rubulavirus mumps).

Picornaviridae

[edit | edit source]
Isosurface shows the capsid of human rhinovirus 14, one of the viruses which cause the common cold. Credit: Thomas Splettstoesser.{{free media}}
Transmission electron microscopy (TEM) micrograph of poliovirus virions. Credit: F.P. Williams, U.S. EPA.{{free media}}

The three species of Enterovirus (rhinovirus) (A, B, and C) include around 160 recognized types of human rhinovirus that differ according to their surface proteins (serotypes).[73]

When a cluster of nurses developed a mild respiratory illness, Winston Price, from the Johns Hopkins University, took nasal passage samples and isolated the first rhinovirus, which he called the JH virus, named after Johns Hopkins.[74][75] His findings were published in 1956.[76]

The seasonality may be due to the start of the school year in the Southern Hemisphere in January, yet colds are still predominant in autumn & winter and to people spending more time indoors thereby increasing the chance of transmission of the virus.[77] Lower ambient temperatures, especially outdoors, may also be factor[78] given that rhinoviruses preferentially replicate at 32 °C (89 °F) as opposed to 37 °C (98 °F).

A poliovirus, the causative agent of polio (also known as poliomyelitis), is a serotype of the species Enterovirus C, in the family of Picornaviridae.[79] There are three poliovirus serotypes: types 1, 2, and 3.

Poxviridae

[edit | edit source]
Diagram shows the structural protein of the genus Orthopoxvirus. Credit: ViralZone, SIB Swiss Institute of Bioinformatics.{{free media}}

Diseases associated with this genus include smallpox, cowpox, horsepox, camelpox, and monkeypox.[80][20]

The most widely known member of the genus is Variola virus, which causes smallpox, eradicated globally by 1977, through the use of Vaccinia virus as a vaccine, where the most recently described species is the Alaskapox virus, first isolated in 2015.[81]

Predicting the phylogeny by sequence or by gene content produces somewhat different results:[82]

Orthopoxvirus phylogeny
By sequence By gene content Genus species Common name
Ectromelia virus Ectromelia virus Orthopoxvirus ectromelia mousepox
Cowpox virus, Germany and Brighton Cowpox virus Orthopoxvirus cowpox cowpox
Taterapox virus, Camelpox virus, Variola virus Horsepox
Monkeypox virus Vaccinia, including rabbitpox
Cowpox virus, GRI strain Variola virus
Vaccinia virus, including rabbitpox and horsepox Taterapox virus, Camelpox virus, Monkeypox virus

Some of the differences in the two trees are attributed to the procedure of passage in producing vaccinia strains. The MVA (Ankara) strain in this regard has a lot of gene loss related to in vitro passage, and horsepox being a vaccinia strain found in a natural outbreak has less.[82]

Based on the genome organisation and DNA replication mechanism it seems that phylogenetic relationships may exist between the rudiviruses (Rudiviridae) and the large eukaryal DNA viruses: the African swine fever virus (Asfarviridae), Chlorella viruses (Phycodnaviridae) and poxviruses (Poxviridae).[83]

Quokkapox virus (QPV), also known as quokka poxvirus, marsupial papillomavirus, or marsupialpox virus[84] is a DNA virus#Group I: dsDNA viruses which is the cause of quokka pox. It is unclear whether this virus is its own species or a member of another species.[85] It primarily infects the quokka, which is one of only four Macropodidae (macropodid) marsupials to get pox lesions. The lesions can mainly be seen on the tail, and can be up to 5 centimetres (2.0 in) in diameter.[86]

Because the quokka host primarily lives on isolated islands in Western Australia, the range of the virus is limited as well. It was first described in 1972 from samples taken on Rottnest Island.[87]

See also

[edit | edit source]

References

[edit | edit source]
  1. ↑ Widsith (30 September 2007). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  2. ↑ DCDuring (16 December 2014). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  3. ↑ Jag123 (9 March 2005). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  4. ↑ 76.170.61.171 (15 August 2009). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  5. ↑ CGP~enwiktionary (20 June 2004). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  6. ↑ Quercus solaris (2 April 2021). "virus". San Francisco, California: Wikimedia Foundation, Inc. Retrieved 17 February 2022. {{cite web}}: |author= has generic name (help)
  7. ↑ Wu KJ (15 April 2020). "There are more viruses than stars in the universe. Why do only some infect us? – More than a quadrillion quadrillion individual viruses exist on Earth, but most are not poised to hop into humans. Can we find the ones that are?". National Geographic Society. Retrieved 18 May 2020.
  8. ↑ Koonin EV, Senkevich TG, Dolja VV (September 2006). "The ancient Virus World and evolution of cells". Biology Direct 1 (1): 29. doi:10.1186/1745-6150-1-29. PMID 16984643. PMC 1594570. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1594570/. 
  9. ↑ Zimmer Carl (26 February 2021). "The Secret Life of a Coronavirus - An oily, 100-nanometer-wide bubble of genes has killed more than two million people and reshaped the world. Scientists don't quite know what to make of it". Retrieved 28 February 2021. {{cite web}}: |archive-date= requires |archive-url= (help)
  10. ↑ Dimmock NJ, Easton AJ, Leppard K (2007). Introduction to Modern Virology (Sixth ed.). Blackwell Publishing. 
  11. ↑ "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses. Retrieved 21 May 2021.
  12. ↑ Breitbart Mya, Rohwer F (June 2005). "Here a virus, there a virus, everywhere the same virus?". Trends in Microbiology 13 (6): 278–84. doi:10.1016/j.tim.2005.04.003. PMID 15936660. 
  13. ↑ Lawrence CM, Menon S, Eilers BJ, Bothner B, Khayat R, Douglas T, Young MJ (May 2009). "Structural and functional studies of archaeal viruses". The Journal of Biological Chemistry 284 (19): 12599–603. doi:10.1074/jbc.R800078200. PMID 19158076. PMC 2675988. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2675988/. 
  14. ↑ Edwards RA, Rohwer F (June 2005). "Viral metagenomics". Nature Reviews. Microbiology 3 (6): 504–10. doi:10.1038/nrmicro1163. PMID 15886693. 
  15. ↑ Robilotti E, Deresinski S, Pinsky BA (January 2015). "Norovirus". Clinical Microbiology Reviews 28 (1): 134–64. doi:10.1128/CMR.00075-14. PMID 25567225. PMC 4284304. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4284304/. 
  16. ↑ 16.0 16.1 Shors T (2017). Understanding Viruses. Jones and Bartlett Publishers. 
  17. ↑ D'Herelle F (September 2007). "On an invisible microbe antagonistic toward dysenteric bacilli: brief note by Mr. F. D'Herelle, presented by Mr. Roux. 1917". Research in Microbiology 158 (7): 553–54. doi:10.1016/j.resmic.2007.07.005. PMID 17855060. 
  18. ↑ 18.0 18.1 18.2 18.3 18.4 18.5 18.6 18.7 18.8 "9.11H: Double-Stranded DNA Viruses- Adenoviruses". Biology LibreTexts. 25 June 2017. https://bio.libretexts.org/Bookshelves/Microbiology/Book%3A_Microbiology_(Boundless)/9%3A_Viruses/9._11%3A_DNA_Viruses_in_Eukaryotes/9.11H%3A_Double-Stranded_DNA_Viruses-_Adenoviruses#:~:text=Siadenovirus%2C%20and%20Ichtadenovirus.-,Genome,larger%20than%20other%20dsDNA%20viruses.. Retrieved 6 January 2021. 
  19. ↑ Rowe Wallace P., Huebner Robert J, Gilmore LK, Parrott RH, Ward TG (December 1953). "Isolation of a cytopathogenic agent from human adenoids undergoing spontaneous degeneration in tissue culture". Proceedings of the Society for Experimental Biology and Medicine 84 (3): 570–3. doi:10.3181/00379727-84-20714. PMID 13134217. 
  20. ↑ 20.0 20.1 "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Retrieved 22 May 2021.
  21. ↑ Dhingra A, Hage E, Ganzenmueller T, Böttcher S, Hofmann J, Hamprecht K, Obermeier P, Rath B, Hausmann F, Dobner T, Heim A (January 2019). "Molecular Evolution of Human Adenovirus (HAdV) Species C". Scientific Reports 9 (1): 1039. doi:10.1038/s41598-018-37249-4. PMID 30705303. PMC 6355881. //www.ncbi.nlm.nih.gov/pmc/articles/PMC6355881/. 
  22. ↑ Walsh MP, Seto J, Liu EB, Dehghan S, Hudson NR, Lukashev AN, Ivanova O, Chodosh J, Dyer DW, Jones MS, Seto D (October 2011). "Computational analysis of two species C human adenoviruses provides evidence of a novel virus". Journal of Clinical Microbiology 49 (10): 3482–90. doi:10.1128/JCM.00156-11. PMID 21849694. PMC 3187342. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3187342/. 
  23. ↑ Robinson CM, Singh G, Henquell C, Walsh MP, Peigue-Lafeuille H, Seto D, Jones MS, Dyer DW, Chodosh J (January 2011). "Computational analysis and identification of an emergent human adenovirus pathogen implicated in a respiratory fatality". Virology 409 (2): 141–7. doi:10.1016/j.virol.2010.10.020. PMID 21056888. PMC 3006489. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3006489/. 
  24. ↑ Singh G, Robinson CM, Dehghan S, Schmidt T, Seto D, Jones MS, Dyer DW, Chodosh J (April 2012). "Overreliance on the hexon gene, leading to misclassification of human adenoviruses". Journal of Virology 86 (8): 4693–5. doi:10.1128/jvi.06969-11. PMID 22301156. PMC 3318657. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3318657/. 
  25. ↑ Singh G, Zhou X, Lee JY, Yousuf MA, Ramke M, Ismail AM, Lee JS, Robinson CM, Seto D, Dyer DW, Jones MS, Rajaiya J, Chodosh J (November 2015). "Recombination of the epsilon determinant and corneal tropism: Human adenovirus species D types 15, 29, 56, and 69". Virology 485: 452–9. doi:10.1016/j.virol.2015.08.018. PMID 26343864. PMC 4619159. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4619159/. 
  26. ↑ Jones MS, Harrach B, Ganac RD, Gozum MM, Dela Cruz WP, Riedel B, Pan C, Delwart EL, Schnurr DP (June 2007). "New adenovirus species found in a patient presenting with gastroenteritis". Journal of Virology 81 (11): 5978–84. doi:10.1128/JVI.02650-06. PMID 17360747. PMC 1900323. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1900323/. 
  27. ↑ "Adenovirus Home CDC". www.cdc.gov. Centers for Disease control and prevention. 31 January 2020. Retrieved 6 January 2021.
  28. ↑ Voss JD, Atkinson RL, Dhurandhar NV (November 2015). "Role of adenoviruses in obesity". Reviews in Medical Virology 25 (6): 379–87. doi:10.1002/rmv.1852. PMID 26352001. https://zenodo.org/record/1229348. 
  29. ↑ Harrach B, Benkő M (2021). Adenoviruses (Adenoviridae), In: Encyclopedia of Virology. 2. Elsevier. https://books.google.com/books?id=m-T7DwAAQBAJ. Retrieved 12 March 2021. 
  30. ↑ Reddy VS, Natchiar SK, Stewart PL, Nemerow GR (August 2010). "Crystal structure of human adenovirus at 3.5 A resolution". Science 329 (5995): 1071–5. doi:10.1126/science.1187292. PMID 20798318. PMC 2929978. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2929978/. 
  31. ↑ "Scientists unveil structure of adenovirus, the largest high-resolution complex ever found". Science Daily. August 28, 2010.
  32. ↑ Harrison SC (August 2010). "Virology. Looking inside adenovirus". Science 329 (5995): 1026–7. doi:10.1126/science.1194922. PMID 20798308. 
  33. ↑ 33.0 33.1 Dixon (2008). "African Swine Fever Virus". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN 978-1-904455-22-6. https://www.caister.com/avir. 
  34. ↑ Denyer, M. S.; Wilkinson, P. J. (1998). "African Swine Fever". Encyclopedia of Immunology. p. 54. doi:10.1006/rwei.1999.0015. ISBN 9780122267659. https://archive.org/details/encyclopediaofim00delv/page/54. 
  35. ↑ "African swine fever". European Food Safety Authority. Retrieved 26 April 2019.
  36. ↑ Smriti Mallapaty (25 April 2019). "Spread of deadly pig virus in China hastens vaccine research". Nature 569 (7754): 13–14. doi:10.1038/d41586-019-01269-5. PMID 31040406. 
  37. ↑ Gaudreault, Natasha N.; Madden, Daniel W.; Wilson, William C.; Trujillo, Jessie D.; Richt, Juergen A. (2020). "African Swine Fever Virus: An Emerging DNA Arbovirus". Frontiers in Veterinary Science 7: 215. doi:10.3389/fvets.2020.00215. PMID 32478103. PMC 7237725. //www.ncbi.nlm.nih.gov/pmc/articles/PMC7237725/. 
  38. ↑ "ICTV Taxonomy history: Orthocoronavirinae". International Committee on Taxonomy of Viruses (ICTV). Retrieved 24 January 2020.
  39. ↑ Fan Y, Zhao K, Shi ZL, Zhou P (March 2019). "Bat Coronaviruses in China". Viruses 11 (3): 210. doi:10.3390/v11030210. PMID 30832341. PMC 6466186. //www.ncbi.nlm.nih.gov/pmc/articles/PMC6466186/. 
  40. ↑ Cherry J, Demmler-Harrison GJ, Kaplan SL, Steinbach WJ, Hotez PJ (2017). Feigin and Cherry's Textbook of Pediatric Infectious Diseases. Elsevier Health Sciences. p. PT6615. https://books.google.com/books?id=z-ZIDwAAQBAJ&pg=PT6615. 
  41. ↑ 41.0 41.1 Woo PC, Huang Y, Lau SK, Yuen KY (August 2010). "Coronavirus genomics and bioinformatics analysis". Viruses 2 (8): 1804–20. doi:10.3390/v2081803. PMID 21994708. PMC 3185738. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3185738/. 
  42. ↑ 42.0 42.1 Almeida JD, Berry DM, Cunningham CH, Hamre D, Hofstad MS, Mallucci L, McIntosh K, Tyrrell DA (November 1968). "Virology: Coronaviruses". Nature 220 (5168): 650. doi:10.1038/220650b0. PMC 7086490. //www.ncbi.nlm.nih.gov/pmc/articles/PMC7086490/. 
  43. ↑ "ICTV Taxonomy history: Human alphaherpesvirus 3". International Committee on Taxonomy of Viruses (ICTV). Retrieved 9 January 2019.
  44. ↑ "ICTV 9th Report (2011) Herpesviridae". International Committee on Taxonomy of Viruses (ICTV). Retrieved 9 January 2019. Human herpesvirus 3 Human herpesvirus 3 [X04370=NC_001348] (HHV-3) (Varicella-zoster virus)
  45. ↑ "Pathogen Safety Data Sheets: Infectious Substances – Varicella-zoster virus". canada.ca. Pathogen Regulation Directorate, Public Health Agency of Canada. 2012-04-30. Retrieved 2017-10-10.
  46. ↑ Nagel MA, Gilden DH (July 2007). "The protean neurologic manifestations of varicella-zoster virus infection". Cleveland Clinic Journal of Medicine 74 (7): 489–94, 496, 498-9 passim. doi:10.3949/ccjm.74.7.489. PMID 17682626. 
  47. ↑ Steiner I, Kennedy PG, Pachner AR (November 2007). "The neurotropic herpes viruses: herpes simplex and varicella-zoster". The Lancet. Neurology 6 (11): 1015–28. doi:10.1016/S1474-4422(07)70267-3. PMID 17945155. 
  48. ↑ 48.0 48.1 Tortora G. Microbiology: An Introduction. Pearson. pp. 601–602. 
  49. ↑ Harpaz, R; Ortega-Sanchez, IR; Seward, JF (6 June 2008). "Prevention of herpes zoster: recommendations of the Advisory Committee on Immunization Practices (ACIP)". Morbidity and Mortality Weekly Report (MMWR) 57 (RR-5): 1-30; quiz CE2-4. PMID 18528318. 
  50. ↑ Pinchinat, Sybil; Cebrián-Cuenca, Ana M; Bricout, Hélène; Johnson, Robert W (December 2013). "Similar herpes zoster incidence across Europe: results from a systematic literature review". BMC Infectious Diseases 13 (1): 170. doi:10.1186/1471-2334-13-170. PMID 23574765. PMC 3637114. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3637114/. 
  51. ↑ Nilsson, Jonas; Cassel, Tobias; Lindquist, Lars (22 May 2015). "Burden of herpes zoster and post-herpetic neuralgia in Sweden". BMC Infectious Diseases 15: 215. doi:10.1186/s12879-015-0951-7. PMID 26002038. PMC 4493830. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4493830/. 
  52. ↑ Becerra JC, Sieber R, Martinetti G, Costa ST, Meylan P, Bernasconi E (July 2013). "Infection of the central nervous system caused by varicella zoster virus reactivation: a retrospective case series study". International Journal of Infectious Diseases 17 (7): e529-34. doi:10.1016/j.ijid.2013.01.031. PMID 23566589. 
  53. ↑ Nagel MA, Cohrs RJ, Mahalingam R, Wellish MC, Forghani B, Schiller A, Safdieh JE, Kamenkovich E, Ostrow LW, Levy M, Greenberg B, Russman AN, Katzan I, Gardner CJ, Häusler M, Nau R, Saraya T, Wada H, Goto H, de Martino M, Ueno M, Brown WD, Terborg C, Gilden DH (March 2008). "The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features". Neurology 70 (11): 853–60. doi:10.1212/01.wnl.0000304747.38502.e8. PMID 18332343. PMC 2938740. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2938740/. 
  54. ↑ Han DH (25 October 2017). "General Characteristics and Epidemiology of varicella-zoster virus (VZV)". The Lecturio Medical Concept Library. Medical Professionals Reference (MPR). Retrieved 2021-06-14.
  55. ↑ Davison AJ, Scott JE (September 1986). "The complete DNA sequence of varicella-zoster virus". The Journal of General Virology 67 ( Pt 9) (9): 1759–816. doi:10.1099/0022-1317-67-9-1759. PMID 3018124. 
  56. ↑ Chow VT, Tipples GA, Grose C (August 2013). "Bioinformatics of varicella-zoster virus: single nucleotide polymorphisms define clades and attenuated vaccine genotypes". Infection, Genetics and Evolution 18: 351–6. doi:10.1016/j.meegid.2012.11.008. PMID 23183312. PMC 3594394. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3594394/. 
  57. ↑ Grose C (September 2012). "Pangaea and the Out-of-Africa Model of Varicella-Zoster Virus Evolution and Phylogeography". Journal of Virology 86 (18): 9558–65. doi:10.1128/JVI.00357-12. PMID 22761371. PMC 3446551. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3446551/. 
  58. ↑ 58.0 58.1 Loparev VN, Rubtcova EN, Bostik V, Tzaneva V, Sauerbrei A, Robo A, Sattler-Dornbacher E, Hanovcova I, Stepanova V, Splino M, Eremin V, Koskiniemi M, Vankova OE, Schmid DS (January 2009). "Distribution of varicella-zoster virus (VZV) wild-type genotypes in northern and southern Europe: evidence for high conservation of circulating genotypes". Virology 383 (2): 216–25. doi:10.1016/j.virol.2008.10.026. PMID 19019403. 
  59. ↑ Zell R, Taudien S, Pfaff F, Wutzler P, Platzer M, Sauerbrei A (February 2012). "Sequencing of 21 varicella-zoster virus genomes reveals two novel genotypes and evidence of recombination". Journal of Virology 86 (3): 1608–22. doi:10.1128/JVI.06233-11. PMID 22130537. PMC 3264370. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3264370/. 
  60. ↑ Loparev VN, Rubtcova EN, Bostik V, Govil D, Birch CJ, Druce JD, Schmid DS, Croxson MC (December 2007). "Identification of five major and two minor genotypes of varicella-zoster virus strains: a practical two-amplicon approach used to genotype clinical isolates in Australia and New Zealand". Journal of Virology 81 (23): 12758–65. doi:10.1128/JVI.01145-07. PMID 17898056. PMC 2169114. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2169114/. 
  61. ↑ McGeoch DJ, Cook S (April 1994). "Molecular phylogeny of the alphaherpesvirinae subfamily and a proposed evolutionary timescale". Journal of Molecular Biology 238 (1): 9–22. doi:10.1006/jmbi.1994.1264. PMID 8145260. 
  62. ↑ Bennett AJ, Paskey AC, Ebinger A, Kuhn JH, Bishop-Lilly KA, Beer M, Goldberg TL (31 July 2020). "Create two new species and rename one species in genus Rubivirus (Hepelivirales: Matonaviridae)". International Committee on Taxonomy of Viruses (ICTV). Retrieved 15 May 2021.{{cite web}}: CS1 maint: uses authors parameter (link)
  63. ↑ 63.0 63.1 63.2 ICTV. "Create a new family Matonaviridae to include the genus Rubivirus, removed from the family Togaviridae Release". Retrieved 29 October 2019.
  64. ↑ 64.0 64.1 Dominguez G, Wang CY, Frey TK (July 1990). "Sequence of the genome RNA of rubella virus: evidence for genetic rearrangement during togavirus evolution". Virology 177 (1): 225–38. doi:10.1016/0042-6822(90)90476-8. PMID 2353453. PMC 7131718. //www.ncbi.nlm.nih.gov/pmc/articles/PMC7131718/. 
  65. ↑ Chen, MH; Frey TK (1999). "Mutagenic analysis of the 3' cis-acting elements of the rubella virus genome". Journal of Virology 73 (4): 3386–3403. PMID 10074193. PMC 104103. //www.ncbi.nlm.nih.gov/pmc/articles/PMC104103/. 
  66. ↑ Zhou Y, Chen X, Ushijima H, Frey TK (2012) Analysis of base and codon usage by rubella virus. Arch Virol
  67. ↑ Dan Dou, Rebecca Revol, Henrik Östbye, Hao Wang, and Robert Daniels (20 July 2018). "Influenza A Virus Cell Entry, Replication, Virion Assembly and Movement". Frontiers in Immunology 9: 1581. doi:10.3389/fimmu.2018.01581. https://www.frontiersin.org/articles/10.3389/fimmu.2018.01581/full. Retrieved 22 February 2022. 
  68. ↑ "Viral Zone". ExPASy. Retrieved 15 June 2015.
  69. ↑ "Paramyxoviridae - Paramyxoviridae - Negative-sense RNA Viruses - ICTV". Retrieved 2020-12-14.
  70. ↑ Fields virology. Fields, Bernard N., Knipe, David M. (David Mahan), 1950-, Howley, Peter M. (6th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2013. pp. 883. OCLC 825740706. 
  71. ↑ Samal, SK, ed (2011). The Biology of Paramyxoviruses. Caister Academic Press. ISBN 978-1-904455-85-1. 
  72. ↑ "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Retrieved 18 May 2021.
  73. ↑ Nicola Davison (6 October 2017). "Why can't we cure the common cold?", The Guardian
  74. ↑ Offit, Paul A. (2007). Vaccinated; One man's quest to defeat the world's deadliest diseases. HarperCollins. pp. 66–68. https://www.academia.edu/28168473. 
  75. ↑ Public Health Reports. 74. The Service. 1959. p. 9. https://books.google.com/books?id=XFZ6ZQDXb0QC&pg=PA9. 
  76. ↑ Kennedy, Joshua L; Turner, Ronald B.; Braciale, Thomas; Heymann, Peter W.; Borish, Larry (June 2012). "Pathogenesis of Rhinovirus Infection". Current Opinion in Virology 2 (3): 287–293. doi:10.1016/j.coviro.2012.03.008. ISSN 1879-6257. PMID 22542099. PMC 3378761. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3378761/. 
  77. ↑ Kolinski, John M.; Schneider, Tobias M. (2021). "Superspreading events suggest aerosol transmission of SARS-CoV-2 by accumulation in enclosed spaces". Physical Review E 103 (3): 033109. doi:10.1103/PhysRevE.103.033109. PMID 33862829. 
  78. ↑ "Temperature-dependent innate defense against the common cold virus limits viral replication at warm temperature in mouse airway cells". Proceedings of the National Academy of Sciences of the United States of America 112 (3): 827–32. January 2015. doi:10.1073/pnas.1411030112. PMID 25561542. PMC 4311828. //www.ncbi.nlm.nih.gov/pmc/articles/PMC4311828/. 
  79. ↑ Ryan KJ, Ray CG, ed (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. 
  80. ↑ "Viral Zone". ExPASy. Retrieved 15 June 2015.
  81. ↑ Gigante, Crystal M.; Gao, Jinxin; Tang, Shiyuyun; McCollum, Andrea M.; Wilkins, Kimberly; Reynolds, Mary G.; Davidson, Whitni; McLaughlin, Joseph et al. (August 2019). "Genome of Alaskapox Virus, a Novel Orthopoxvirus Isolated from Alaska". Viruses 11 (8): 708. doi:10.3390/v11080708. PMID 31375015. PMC 6723315. //www.ncbi.nlm.nih.gov/pmc/articles/PMC6723315/. 
  82. ↑ 82.0 82.1 Hendrickson, RC; Wang, C; Hatcher, EL; Lefkowitz, EJ (September 2010). "Orthopoxvirus genome evolution: the role of gene loss.". Viruses 2 (9): 1933–67. doi:10.3390/v2091933. PMID 21994715. PMC 3185746. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3185746/. 
  83. ↑ Prangishvili, D; Garrett, RA (2004). "Exceptionally diverse morphotypes and genomes of crenarchaeal hyperthermophilic viruses". Biochem Soc Trans 32 (2): 204–208. doi:10.1042/bst0320204. PMID 15046572. https://curis.ku.dk/ws/files/51497971/0320204.pdf. 
  84. ↑ Mahy, Brian W. J. (October 2008). The dictionary of virology. Elsevier. pp. 393. https://books.google.com/books?id=ksSkuSLzXJsC. 
  85. ↑ "ICTV 9th Report (2011)". ICTV. Leiden. 2011. Retrieved 30 September 2017. List of other related viruses which may be members of the subfamily Chordopoxvirinae but have not been approved as species Quokka poxvirus
  86. ↑ Williams, Elizabeth S.; Ian K. Barker (2001). Infectious diseases of wild mammals. Blackwell Publishing. pp. 180. doi:10.1002/9780470344880.fmatter. https://books.google.com/books?id=I62ZO_-4cjwC. 
  87. ↑ Papadimitriou, J. M.; Ashman, R. B. (July 1972). "A Poxvirus in a Marsupial Papilloma". Journal of General Virology 16 (1): 87–89. doi:10.1099/0022-1317-16-1-87. PMID 5049081. http://vir.sgmjournals.org/cgi/content/abstract/16/1/87. 
[edit | edit source]
Retrieved from "https://en.wikiversity.org/w/index.php?title=Remedy/Viruses&oldid=2417421"