CAMPAK

Paramyxovirus
From Wikipedia, the free encyclopedia

Paramyxovirus

Virus classification

Group:

Group V ((-)ssRNA)

Order:

Mononegavirales

Family:

Paramyxoviridae

Genera

Subfamily Paramyxovirinae Avulavirus Ferlavirus Henipavirus Morbillivirus Respirovirus Rubulavirus TPMV-like viruses Subfamily Pneumovirinae Pneumovirus Metapneumovirus

Paramyxoviruses (from Greek para-, beyond, -myxo-, mucus or slime, plus virus, from Latin poison, slime) are viruses of the Paramyxoviridae family of theMononegavirales order; they are negative-sense singlestranded RNA viruses responsible for a number of human and animal diseases.[1]
Contents

1 Genera

1.1 Notes

2 Physical structure 3 Genome structure 4 Proteins 5 Pathogenic paramyxoviruses 6 New and emerging paramyxoviruses 7 Evolution 8 See also 9 External links 10 References

[edit]Genera

Subfamily Paramyxovirinae

Genus Aquaparamyxovirus ( type species Atlantic salmon paramyxovirus: others include Pacific salmon paramyxovirus)

Genus Avulavirus (type species Newcastle disease virus) Genus Ferlavirus (Fer-de-Lance virus) Genus Henipavirus (type species Hendravirus; others include Nipahvirus) Genus Morbillivirus (type species Measles virus; others include Rinderpest virus, Canine distemper virus, phocine distemper virus, Ovine rinderpest)

Genus Respirovirus (type species Sendai virus; others include Human parainfluenza viruses 1 and 3, as well some of the viruses of the common cold)

Genus Rubulavirus (type species Mumps virus; others include Achimota virus 1 and 2, Human parainfluenza viruses 2 and 4, Simian parainfluenza virus 5, Menangle virus, Tioman virus,Tuhokovirus 1, 2 and 3)

Genus TPMV-like viruses (type species Tupaia paramyxovirus: other species Mossman virus, Nariva virus and Salem virus)

Species Beilong virus

Subfamily Pneumovirinae

Genus Pneumovirus (type species Human respiratory syncytial virus, others include Bovine respiratory syncytial virus)

Genus Metapneumovirus (type species Avian pneumovirus, Human metapneumovirus)

Unassigned viruses

J virus Sunshine virus Tailam virus

[edit]Notes
The Beilong virus is now known to be a member of the subfamily Paramyxovirinae.[2] It was isolated from rat kidney and its pathogenic potential is unknown. J virus is very similar to Beilong virus and probably belongs in the same genus. Both have features that differ from the other genera in this family. Tailam virus may also belong in this genus. The relations between the salmon paramyxoviruses and the others have been poorly studied to date and their relationship to the other members of this genus is not currently known. Sunshine virus was isolated from pythons in Australia.[3] It appears to be unrelated to other known members of this taxon.

[edit]Physical

structure

Virions are enveloped and can be spherical, filamentous or pleomorphic. Fusion proteins and attachment proteins appear as spikes on the virion surface. Matrix proteins inside the envelope stabilise virus structure. The nucleocapsid core is composed of the genomic RNA, nucleocapsid proteins, phosphoproteins and polymerase proteins.

[edit]Genome

structure

The genome is non-segmented negative-sense RNA, 15-19 kilobases in length and contains 6-10 genes. Extracistronic (non-coding) regions include:

A 3 leader sequence, 50 nucleotides in length, which acts as a transcriptional promoter. A 5 trailer sequence, 50-161 nucleotides long Intergenomic regions between each gene, which are three nucleotides long for morbillivirus, respirovirus and henipavirus, variable length (1-56 nucleotides) for rubulavirus and pneumovirinae.

Each gene contains transcription start/stop signals at the beginning and end, which are transcribed as part of the gene. Gene sequence within the genome is conserved across the family due to a phenomenon known as transcriptional polarity (see Mononegavirales) in which genes closest to the 3 end of the genome are transcribed in greater abundance than those towards the 5 end. This is a result of structure of the genome. After each gene is transcribed, the RNA-Dependent RNA polymerase pauses to release the new mRNA when it encounters an intergenic sequence. When the RNA polymerase is paused, there is a chance that it will

dissociate from the RNA genome. If it dissociates, it must reenter the genome at the leader sequence, rather than continuing to transcribe the length of the genome. The result is that the further downstream genes are from the leader sequence, the less they will be transcribed by RNA polymerase. Evidence for a single promoter model was verified when viruses were exposed to UV light. UV radiation can cause dimerization of RNA, which prevents transcription by RNA polymerase. If the viral genome follows a multiple promoter model, the level inhibition of transcription should correlate with the length of the RNA gene. However, the genome was best described by a single promoter model. When paramyxovirus genome was exposed to UV light, the level of inhibition of transcription was proportional to the distance from the leader sequence. That is, the further the gene is from the leader sequence, the greater the chance of RNA dimerization inhibiting RNA polymerase. The virus takes advantage of the single promoter model by having its genes arranged in relative order of protein needed for successful infection. For example, nucleocapsid protein, N, is needed in greater amounts than RNA polymerase, L. Many Paramyxovirus genomes follow the Rule of Six. The total length of the genome is almost always a multiple of six. This is probably due to the advantage of having all RNA bound by N protein (since N binds hexamers of RNA). If RNA is left exposed, the virus does not replicate efficiently. Members of the sub-family Pneumovirinae do not follow this rule The gene sequence is:

Nucleocapsid Phosphoprotein Matrix Fusion Attachment Large (polymerase)

[edit]Proteins
N the nucleocapsid protein associates with genomic RNA (one molecule per hexamer) and protects the RNA from nuclease digestion

P the phosphoprotein binds to the N and L proteins and forms part of the RNA polymerase complex M the matrix protein assembles between the envelope and the nucleocapsid core, it organizes and maintains virion structure

F the fusion protein projects from the envelope surface as a trimer, and mediates cell entry by inducing fusion between the viral envelope and the cell membrane by class I fusion. One of the defining characteristics of members of the paramyxoviridae family is the requirement for a neutral pH for fusogenic activity.

H/HN/G the cell attachment proteins span the viral envelope and project from the surface as spikes. They bind to proteins on the surface of target cells to facilitate cell entry. Proteins are designated H (hemagglutinin) for morbilliviruses as they possess haemagglutination activity, observed as an ability to

cause red blood cells to clump in laboratory tests. HN (Hemagglutinin-neuraminidase) attachment proteins occur in respiroviruses, rubulaviruses and avulaviruses. These possess both haemagglutination and neuraminidase activity, which cleaves sialic acid on the cell surface, preventing viral particles from reattaching to previously infected cells. Attachment proteins with neither haemagglutination nor neuraminidase activity are designated G (glycoprotein). These occur in members of pneumovirinae and Henipaviruses.

L the large protein is the catalytic subunit of RNA-dependent RNA polymerase (RDRP) Accessory proteins a mechanism known as RNA editing (see Mononegavirales) allows multiple proteins to be produced from the P gene. These are not essential for replication but may aid in survival in vitro or may be involved in regulating the switch from mRNA synthesis to antigenome synthesis.

[edit]Pathogenic

paramyxoviruses

A number of important human diseases are caused by paramyxoviruses. These include mumps, measles, which caused 745,000 deaths in 2001 and respiratory syncytial virus (RSV), which is the major cause of bronchiolitis and pneumonia in infants and children. The parainfluenza viruses are the second most common causes of respiratory tract disease in infants and children. They can cause pneumonia, bronchitis and croup in children and the elderly. Human metapneumovirus, initially described in about 2001, is also implicated in bronchitis, especially in children. Though it was discovered in 2001 it was proven to be circulating in the population for at least 50 years and that by the age of five most children have already been exposed to it.[4] Paramyxoviruses are also responsible for a range of diseases in other animal species, for example canine distemper virus (dogs), phocine distemper virus (seals), cetacean morbillivirus (dolphinsand porpoises), Newcastle disease virus (birds), and rinderpest virus (cattle). Some paramyxoviruses such as the henipaviruses are zoonotic pathogens, occurring naturally in an animal host, but also able to infect humans. Hendra virus (HeV) and Nipah virus (NiV) in the genus Henipavirus have emerged in humans and livestock in Australia and Southeast Asia. Both viruses are contagious, highly virulent, and capable of infecting a number of mammalian species and causing potentially fatal disease. Due to the lack of a licensed vaccine or antiviral therapies, HeV and NiV are designated as biosafety level (BSL) 4 agents. The genomic structure of both viruses is that of a typical paramyxovirus.[5]

[edit]New

and emerging paramyxoviruses

Phylogenetic tree based on the N protein sequences of selected paramyxoviruses. Virus names as follows: Avian paramyxovirus 6 (APMV6); Atlantic salmon paramyxovirus; Beilong virus (BeiPV) ; Bovine parainfluenza virus 3 (bPIV3); Canine distemper virus (CDV); Cedar virus (CedPV); Fer-de-lance virus (FdlPV) ; Hendra virus (HeV); Human parainfluenza virus 2 (hPIV2); Human parainfluenza virus 3 (hPIV3) ; Human parainfluenza virus 4a (hPIV4a) ; Human parainfluenza virus 4b (hPIV4b); J virus (JPV); Menangle virus (MenPV); Measles virus (MeV); Mossman virus (MosPV); Mapeura virus (MprPV); Mumps virus (MuV); Newcastle disease virus (NDV); Nipah virus, Bangladesh strain (NiV-B); Nipah virus, Malaysian strain (NiV-M); Parainfluenza virus 5 (PIV5); Peste-des-petits-ruminants (PPRV); Porcine rubulavirus (PorPV); Rinderpest virus (RPV); Salem virus (SalPV); Sendai virus (SeV); Simian virus 41 (SV41); Tioman virus (TioPV); Tupaia paramyxovirus (TupPV). [6]

The family Paramyxoviridae is composed of a diverse group of viruses and is divided into two subfamilies, Paramyxovirinae and Pneumovirinae. There are currently 40 virus species classified within the Paramyxovirinae subfamily, but several remain unclassified at the genus level. In the past few decades, paramyxoviruses have been discovered from terrestrial, volant and aquatic animals, demonstrating a vast host range and great viral genetic diversity. As molecular technology advances and viral surveillance programs are implemented, the discovery of new viruses in this group is increasing.[1]

[edit]Evolution
The evolution of this group is still debated. Using the pneumovirus as an outgroup, the Paramyxovirinae can be divided into two clades: one with the avulaviruses and rubulaviruses and the other with the respiroviruses, the henipaviruses and the morbilliviruses.[7] Within the second clade the respiroviruses appear to be the basal group. The respirovirus-henipavirus-morbillivirus may be basal to the avulavirus-rubulavirus clade.

[edit]See

also

Animal viruses Virology Henipavirus

[edit]External

links

Paramyxoviruses (1998) morphology, genome, replication, pathogenesis (special access required) Hendra virus has a growing family tree (2001) CSIRO Paramyxovirus press release Animal viruses Paramyxoviridae Genomes Viral Bioinformatics Resource Center Viralzone: Paramyxoviridae Virus Pathogen Database and Analysis Resource (ViPR): Paramyxoviridae

[edit]References
a b

1.

Samal, SK (editor) (2011). The Biology of Paramyxoviruses. Caister Academic Press. ISBN 978-1-

904455-85-1. 2. ^ Woo PC, Lau SK, Wong BH, Wu Y, Lam CS, Yuen KY (2012) Novel variant of beilong paramyxovirus in rats, China. Emerg Infect Dis 18(6):1022-1024 doi: 10.3201/eid1806.111901. 3. ^ Hyndman TH, Marschang RE, Wellehan JF Jr, Nicholls PK (2012) Isolation and molecular identification of sunshine virus, a novel paramyxovirus found in Australian snakes. Infect Genet Evol 4. ^ Harnden, Anthony. "Human metapneumovirus". British Journal of General Practice. Retrieved 20 September 2012. 5. ^ Sawatsky (2008). "Hendra and Nipah Virus". Animal Viruses: Molecular Biology. Caister Academic Press. ISBN [[Special:BookSources/978-1-904455-22-6]|978-1-904455-22-6]]]. [http://www.horizonpress.com/avir. 6. ^ Marsh GA, de Jong C, Barr JA, Tachedjian M, Smith C, Middleton D, Yu M, Todd S, Foord AJ, Haring V, Payne J, Robinson R, Broz I, Crameri G, Field HE, Wang LF (2012). "Cedar virus: a novel Henipavirus isolated from Australian bats". PLoS Pathogens 8 (8): e1002836. doi:10.1371/journal.ppat.1002836. PMC 3410871. PMID 22879820. 7. ^ McCarthy AJ, Goodman SJ (2010) Reassessing conflicting evolutionary histories of the Paramyxoviridae and the origins of respiroviruses with Bayesian multigene phylogenies. Infect Genet Evol 10(1):97-107

Taken from: http://en.wikipedia.org/wiki/Paramyxovirus

Taken from: http://pathmicro.med.sc.edu/mhunt/RNA10.jpg

GENERAL INFORMATION

back to top

Paramyxoviruses are an important class of viruses which are associated with respiratory ailments, and common childhood diseases such as measles and mumps. Paramyxoviruses are a significant cause of morbidity and mortality globally, especially in children and the elderly.

TAXONOMY
FAMILY: Paramyxoviridae SUBFAMILY GENUS SPECIES

back to top

Paramyxovirinae Paramyxovirus Human Parainfluenza Virus type 1,3 Paramyxovirinae Rubulavirus Paramyxovirinae Morbilivirus Paramyxovirinae Henipavirus Pneumovirinae Pneumovirus Human Parainfluenza Virus type 2, 4a, 4b , Mumps virus Measles virus Hendravirus, Nipahvirus Respiratory Syncytial Virus

MORPHOLOGY
Morphology

back to top

Paramyxoviruses encode negative-sense, single-stranded, monopartite RNA. They are enveloped and contain a helical nucleocapsid. They appear pleomorphic or spherical in electron micrographs.

REPLICATION STRATEGY

back to top

-ssRNA must first be converted into +ssRNA (mRNA) by the RNA-dependent RNA polymerase (RDRP) incorporated in the virion. The mRNA can then be translated into proteins. Replicative enzymes (RDRP) synthesize a negative-strand copy of the +RNA. Structural proteins translated from the mRNA are then used to package progeny -RNA and RDRP into virions.

VIRAL PROFILES

back to top

Measles

Incubation: Normally 8-14 days

Epidemiology: There is only one serotype of measles that causes the disease. Main route of transmission is via inhalation. Recently the prevalence of measles has decreased dramatically in developed nations, but measles is still a problem in third-world nations, especially in Africa and Central and South America. Symptomatology and Outcome

Oral exanthem of Measles infection

Classic non-vesicular exanthem associated with measles

Another classical case of measles exanthem

Symptoms: o Infected person first experiences fever, cough and runny nose. Occasionally includes conjunctivitis, or pink eye. o Maculopapular rash normally appears 14 days into the illness. It starts at the head and moves down the neck to the lower part of the body and to the legs and arms. o Kopliks spots: Irregular, bright-red spots in mucosal membranes with bluish-white speck at center. Complications: o Ear infections: most common complication (1/10 cases) o Pneumonia: Very common complication and cause of mortality in developing countries. As many as 1/5 children with measles in developing countries can contract pneumonia.

Diarrhea Post-infectious Measles Encephalitis: A complication from measles that leads to swelling of the brain that can be accompanied with meningitis. Proceeds from headache, fever and discomfort to loss of motor control, cognitive impairment, occasional seizures, visual loss and death. Can occur between 8 days and a month after infection. Occurs more commonly in children o Sub-Sclerosing Panencephalitis, or SSPE A very rare complication from measles that is associated with a rare form of the virus Can arise anywhere from 1 to 12 years after initial measles infection Usually Fatal Symptoms progress from behavioral changes to loss of motor control and coordination, slurred speech, paralysis and eventually to death. Outcome: o Most people who get measles normally recover. Serious complications, however, are more common in developing nations and in areas where access to healthcare and/or basic care is scarce. o Measles is not normally deadly, but mortality and complications increase dramatically where malnutrition and vitamin A deficiency is common.

o o

Prevention/ Management

Vaccination with the Measles, Mumps and Rubella vaccine is very effective. Prevalence of Measles has significantly decreased in developed nations with successful vaccination programs Vaccine is currently administered in a 2-dose program at 12-15 months and again at 8-12 years of age.

There have been a few adverse effects associated with vaccination, such as pneumonia and atypical measles. Treatment: there is no effective antiviral treatment or therapy for measles.

Taken from: http://www.stanford.edu/group/virus/paramyxo/2005/

General Concepts
Paramyxoviruses The family Paramyxoviridae consists of three genera: Paramyxovirus, which includes the parainfluenza viruses and mumps virus; Pneumovirus, which includes respiratory syncytial virus; and Morbillivirus, which includes the measles virus.
Structure

All paramyxoviruses are enveloped particles 150 to 300 nm in diameter. The tubelike, helically symmetrical nucleocapsid contains a monopartite, single-stranded, negativesense RNA genome and an RNA-directed RNA polymerase. The nucleocapsid associates with the matrix protein (M) at the base of a double-layered lipid envelope. The spikes on the envelope contain two glycoproteins, a viral attachment protein, and a fusion protein. The paramyxoviruses can be distinguished by the gene order for the viral proteins and by the biochemical properties for their viral attachment proteins. In parainfluenza viruses, the viral protein spikes have hemagglutinating and neuraminidase activities (HN). Respiratory syncytial virus lacks both these activities and measles virus lacks neuraminidase but has hemagglutinating activity. All paramyxoviruses are labile to very labile and quickly inactivated, e.g. by heat, organic solvents, detergents, ultraviolet, or visible light, and low pH value.
Multiplication

The multiplication of all paramyxoviruses is similar to that of orthomyxoviruses except that the paramyxovirus genome is monopartite. Parainfluenza Viruses
Clinical Manifestations

Parainfluenza viruses cause mild or severe upper and lower respiratory tract infections, particularly in children.

Classification and Antigenic Types

Human parainfluenza viruses are divided into types 1, 2, 3, and 4; type 4 consists of A and B subtypes.
Pathogenesis

Transmission is by droplets or direct contact. The virus disseminates locally in the ciliated epithelial cells of the respiratory mucosa.
Host Defenses

Nonspecific defenses, including interferon, are followed by the appearance of secretory and humoral antibodies and cell-mediated immune responses.
Epidemiology

Parainfluenza virus diseases occur worldwide; they are usually endemic but sometimes epidemic. Primary infections occur in young children; reinfection is common but results in milder disease.
Diagnosis

Clinical symptoms are nonspecific. Laboratory diagnosis is made by detecting viral antigen, by isolating the virus, or by detecting a rise in antibody titer or elevated IgGand IgA- (IgM-) antibodies in a single serum.
Control

No vaccine is available.
Taken from: http://www.ncbi.nlm.nih.gov/books/NBK8461/
Diskripsi Penyakit ini adalah suatu infeksi virus yang sangat menular, ditandai dengan demam, batuk, pilek, konjungtivitis (peradangan selaput ikat mata/konjungtiva) dan ruam kulit. Penyakit ini biasanya menyerang anak-anak pra sekolah dan anak-anak SD, meskipun tidak menutup kemungkinan menyerang orang dewasa yang belum pernah terkena penyakit ini. Jika orang sudah terkena campak maka sepanjang hidupnya tidak akan terkena penyakit ini lagi. Gejala Gejala-gejala yang nampak pada penderita campak antara lain; demam tinggi, bintik putih pada bagian dalam pipi sebelah depan gigi geraham, mata merah dan berairi, tenggorokan sakit, pilek, batuk kering. Terkadang jika penderitanya anak-anak akan terjadi muntah-muntah, diare, bintik di belakang telinga. Pengobatan Tidak ada pengobatan khusus untuk campak. Namun untuk pencegahan biasanya diberikan vaksin campak rutin kepada anak-anak.

Taken from: http://adesyams.blogspot.com/2010/03/penyakit-campak-gejala-dan.html

Campak : Penyebab, Diagnosis, Gejala, Pencegahan Dan Pengobatan

Sunday, August 12th 2012. | Darah dan Imun, Kesehatan Anak, Penyakit Umum

Campak adalah penyakit yang disebabkan oleh infeksi virus (myxoviruses) yang sangat menular, dan yang menyebabkan gambaran klinis dalam tiga tahap, periode awal inkubasi hampir tidak ada gejala, tahap awal dengan kemerahan intens pada mukosa mulut, tenggorokan dan mata.Setelah tahap awal, bintik-bintik merah pada kulit mulai menyatu membentuk ruam, batuk disertai demam dan kemerahan pada konjungtiva mata.

Penyebab Campak
Penyebab campak adalah virus morbilli dan Paramyxoviridae. Infeksi ini ditularkan melalui sekresi oral atau hidung dari orang yang terinfeksi dan inkubasi tersebut adalah 8 sampai 14 hari sebelum timbulnya gejala. Infektivitas yang tinggi dari pasien yang sedang dimulai atas, maka kurang kuat, juga dieliminasi virus campak selama 5 hari pertama dari periode exanthematous. Penularan terjadi melalui udara. Infeksi dapat menyebabkan epidemi pada musim dingin dan musim semi, tidak ada perbedaan antara jenis kelamin. Setelah penyakit ini sembuh, Pasien akan mendapatkan kekebalan seumur hidupnya.cara lain untuk mendapatkan kekebalan yaitu dengan vaksinasi campak. Anak berusia 1 tahun yang belum di vaksinasi rentang terhadap penyakit campak, begitu pula dengan remaja yang belum melakukan vaksinasi ulang.

Diagnosis Campak
Diagnosis ditetapkan berdasarkan anamnesis dan pemeriksaan fisik, dan Pemeriksaan serologik atau virologik yang positif yaitu bila terdapat demam tinggi terus menerus 38,50 C atau lebih disertai batuk, pilek, nyeri menelan, mata merah dan silau bila kena cahaya (fotofobia), seringkali diikuti diare.Pada tahap ini,muncul kemerahan pada mukosa mulut, dengan bintik-bintik yang muncul pada bagian dalam bibir dan pipi muncul ruam makulopapular yang dimulai pada wajah, belakang telinga, sayap hidung, sekitar mulut dan dagu yang didahului oleh suhu yang meningkat lebih tinggi dari semula. Hal ini mengakibatkan anak mengalami kejang demam. Saat ruam timbul, batuk dan diare bertambah parah sehingga anak mengalami sesak nafas atau dehidrasi.2 sampai 3 hari kemudian ruam makulopapular menjadi lebih besar dan menyatu, demam mereda dan kondisi umum mulai membaik. Pada hari selanjutnya exanthematous mulai untuk membersihkan lesi kulit dan pengelupasan kulit.

Gejala Campak
Gejala awal adalah demam tinggi selama 2 hari pertama. Gejala lain yang sering terjadi adalah rhinitis dan konjungtivitis (peradangan selaput ikat mata) dengan ketidaknyamanan intens dengan cahaya Kemerahan pada konjungtiva dan debit mata kadang-kadang bernanah. Biasanya disertai dengan batuk kering dan iritasi. Mata merah dan bengkak pada kelopak mata.

Pengobatan Campak
Sampai saat ini belum ada pengobatan khusus untuk virus campak melainkan hanya untuk mengurangi gejala-gejalanya.Berikut ini beberapa saran untuk menurunkan gejala-gejala campak : Pasien harus beristirahat dan makan makanan yang bergizi agar kekebalan tubuh meningkat. Gunakan parasetamol cair atau ibuprofen untuk meringankan demam, sakit dan nyeri. Hindari penggunaan aspirin karena dapat menyebabkan Sindrom reye. Gunakan lotion kulit (calamine atau mentol) untuk mengobati rasa gatal Obat batuk bisa sedikit meringankan (Harus sesuai petunjuk dokter)

Pencegahan Campak
Untuk pencegahan, harus di lakukan imunisasi pada anak guna melemahkan virus dan mendapatkan Kekebalan terhadap campak . Imunisasi pada anak biasanya dilakukan pada Usia 9-15 bulan, dalam bentuk vaksin MMR (campak, gondok, dan rubella) dengan vaksinasi ulang pada usia 12 tahun.

Taken from: http://www.pustakakesehatan.com/campak-penyebab-diagnosis-gejala-pencegahandan-pengobatan.html PDF lengkap campak di desktop: http://adulgopar.files.wordpress.com/2009/12/campak.pdf