PARAMYXOVIRUSES Parainfluenzae virus PIV STRUCTURE PIV- transmission through droplet dispersion (Courtesy-American Assoc. as long as the Adv. Of Science) RSV- Structure

PARAMYXOVIRUSES Parainfluenzae virus PIV STRUCTURE PIV- transmission through droplet dispersion (Courtesy-American Assoc. as long as the Adv. Of Science) RSV- Structure

PARAMYXOVIRUSES Parainfluenzae virus PIV STRUCTURE PIV- transmission through droplet dispersion (Courtesy-American Assoc. as long as the Adv. Of Science) RSV- Structure

Hudak, Chris, Contributing Writer has reference to this Academic Journal, PHwiki organized this Journal Family Paramyxoviridae Subfamily Paramyxovirinae: Genes: Morbillivirus – measles virus, Respirovirus (earlier Paramyxovirus) – parainfluenza virus serotypes 1 in addition to 3 Rubulavirus – parainfluenza virus serotypes 2, 4, 4b, mumps virus Subfamily Pneumovirinae Genes: Pneumovirus – RS-virus Metapneumovirus Properties of the Paramyxoviruses A. Structure: The particle has a lipid-containing envelope covered with spikes; a helical ribonucleoprotein nucleocapsid 18 nm in diameter is enclosed. The RNA is a single molecule (MW 5-8 x 106).

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PARAMYXOVIRUSES M protein helical nucleocapsid (RNA minus NP protein) HN/H/G glycoprotein SPIKES polymerase complex lipid bilayer membrane F glycoprotein SPIKES pleomorphic STRUCTURE-PARAMYXOVIRUSES The envelope of paramyxoviruses contains 2 glycoproteins, HN in addition to F, that as long as m spikelike projec­tions from the surface of the viral membrane. These glycoproteins are involved in the early interactions between virus in addition to cell. The larger glycoprotein, HN, has neuraminidase in addition to hemagglutinating activities in addition to is responsible as long as virus adsorption. The other glycoprotein, F, is involved in virus-induced cell fusion in addition to hemolysis in addition to in virus penetration through fusion of viral in addition to cell membranes. The membrane-fusing activity of Ihe F protein is activated by proteolytic cleavage of a precursor (Fo) by a host enzyme to yield 2 disulfide-linked polypeptides (F1 in addition to F2). Only then can viral replication begin.

HN: Larger virus glycoprotein, responsible both as long as hemagglutinatlon in addition to receptor-destroying activities of the virus particle. F: Smaller virus glycoprotein, Involved In cell fusion by these viruses in addition to probably in the entry of the virus Into the cell. F is composed of 2 disulfide bond-linked polypeptides cleaved from a high-molecular-weight precursor. Lipid bilayer: The lipid is cell-derived but probably altered in composition from that of the normal cell. M: Nonglycosylated membrane protein. The HN, F, M, in addition to lipid bilayer can be disrupted, destroying hemolytic activity, in addition to then reassembled without the nucleocapsid, whereupon hemolytic activity is restored. NP: Ribonucleoprotein, the major complement-fixing antigen. There is another small protein of about 47,000 molecular weight whose location in addition to function in the virion are unknown. B. Biologic Properties: 1. Cell fusion. In the course of infection, paramyxoviruses cause cell fusion, long recognized as giant cell as long as mation. This ability to fuse cells is now used as long as the creation of cell hybrids, an important tool in somatic cell genetics. 2. Persistent infection. Most paramyxoviruses can produce a persistent noncytocidal infection of cultured cells. The clinical importance of this property may explain subacute sclerosing panencephalitis (SSPE). 3. Antigenic properties. Measles, canine distemper, in addition to rinderpest viruses have related antigens. Another antigenically related group includes mumps, parainfluenza, in addition to Newcastle disease viruses. C. Replication. The RNA genome of viruses of this group is not infectious in addition to does not function as messenger RNA. Instead, the viral genome is transcribed into shorter RNA molecules that serve as messenger in addition to are complementary to the genome. The paramyxoviruses possess an RNA-dependent RNA polymerase that is a structural component of the virion in addition to produces the initial messenger RNA.

MUMPS (Epidemic Parotitis) Mumps is an acute contagious disease characterized by a nonsuppurative enlargement of one or both of the parotid gl in addition to s, although other organs may also be involved. Properties of the Virus Mumps virus is a typical paramyxovirus. A. Morphology in addition to Biochemical Properties. The mumps virus particle has the typical paramyxovirus morphology. Typical also are the biologic properties of hemagglutination, neuraminidase, in addition to hemolysin. Hemagglutination can be inhibited by specific antisera to mumps virus, in addition to this inhibition can be used to measure antibody responses. Similarly, the nucleocapsid of the virus particle as long as ms the major component of the “S” (soluble) complement-fixing antigen. B. Reactions to Physical in addition to Chemical Agents. The hemagglutinin, the hemolysin, in addition to the infectivity of the virus are destroyed by heating at 56 °C as long as 20 minutes. The skin test antigen in addition to the complement-fixing antigen are more heat-stable. C. Animal Susceptibility in addition to Growth of Virus. In monkeys, mumps can produce a disease that is very much like that in human beings. Parotitis is produced by introducing the virus into Stensen’s duct or directly into the gl in addition to by injection. By the use of fluorescent antibody, the virus has been located in the cytoplasm of acinar cells. The virus grows readily in embryonated eggs in addition to in cell culture. Passage in embryonated eggs reduces pathogenicity as long as humans, in addition to this method was used to obtain a vaccine strain. Mumps virus growing in cell culture produces multinucieated giant cells (syncytia).

D. Skin Test. A skin test antigen as long as determining hypersensitivity to mumps virus is available, A posi­tive test is considered to be erythema in addition to induration greater than 15 mm 24-48 hours after injection. The skin lest is of uncertain value in predicting immune status, since both false positives in addition to false negatives occur frequently. Pathogenesis in addition to Pathology Two theories exist regarding the pathogenesis of mumps. (1) The virus travels from the mouth by way of Stensen ‘s duct to the parotid gl in addition to , where it undergoes primary multiplication. This is followed by a generalized viremia in addition to localization in testes. ovaries, pancreas, thyroid, or brain. (2) Primary replication occurs in the superficial epithelium of the respiratory tract. This is followed by a generalized viremia in addition to simultaneous localization in the salivary gl in addition to s in addition to other organs. Little tissue damage is associated with uncompli­cated mumps. The ducts of the parotid gl in addition to s show desquamation of the epithelium, in addition to polymorphonuclear cells are present in the lumens. There are interstitial edema in addition to lymphocytic infiltration. With severe orchitis, the testis is congested, in addition to punctate hemorrhage as well as degeneration of the epithelium of the seminiferous tubules is observed. Central nervous sys­tem pathology may vary from perivascular edema to inflammatory reaction, glial reaction, hemorrhage, or demyelination. Clinical Features The incubation period is commonly 18-21 days. A prodromal period of malaise in addition to anorexia is followed by rapid enlargement of parotid gl in addition to s as well as other salivary gl in addition to s. Swelling may be confined to one parotid gl in addition to , or one gl in addition to may enlarge several days be as long as e the other. The gl in addition to enlargement is associated with pain, especially when tasting acid sub­stances- The salivary adenitis is commonly accompanied by low-grade fever in addition to lasts as long as approximately a week. The testes in addition to ovaries may be affected, especially after puberty. Twenty percent of males over 13 years of age who are infected with mumps virus develop orchitis, which is often unilateral in addition to does not usually lead to sterility. Because of the lack of elasticity of the tunica albuginea, which does not allow the inflamed testis to swell, atrophy of the testis may follow secondary to pressure necrosis. Secondary sterility does not occur in women because the ovary, which has no such limiting membrane, can swell when inflamed.

Mumps accounts as long as 10-15% of aseptic meningitis observed in the USA in addition to is more common among males than females. Meningoencephalitis usually occurs 5-7 days after the inflammation of the salivary gl in addition to s, but it may occur simultaneously or in the absence of parotitis in addition to is usually self-limiting. The cerebrospinal fluid shows pleocytosis (10-2000//n,L, mostly lymphocytes) that may persist after clinical recovery. Rare complications of mumps include (1) a self-limiting polyarthritis that resolves without residual de as long as mity; (2) pancreatitis associated with Transient hyperglycemia, glycosuria, in addition to steatorrhea (it has been suggested that diabetes mellitus may occasionally fol­low); (3) nephritis; (4) thyroiditis; in addition to (5) unilateral nerve deafness (hearing loss is complete in addition to permanent) . Mumps may be a possible causative agent in the production of aqueductal stenosis in addition to hydrocephalus in children. Injection of mumps virus into suckling hamsters has produced similar lesions.

Laboratory Diagnosis Laboratory studies are not usually required to establish the diagnosis of typical cases. However, mumps can sometimes be confused with enlargement of the parotids due to suppuration, as long as eign bodies in the salivary ducts, tumors, etc. In cases without parotitis, particularly in aseptic meningitis, the laboratory can be helpful in establishing the diagnosis. A. Recovery of Virus: Virus can be isolated from saliva, cerebrospinal fluid, or urine collected within 4 days after onset of illness. After treatment with antibiotics, the specimens are inoculated into monkey kidney cell cultures. Virus growth can be detected in 5-6 days by adsorption of suitable erythrocytes by the infected cells. The isolate can be identified with specific antiserum that can inhibit the hemadsorption. Immunofluorescent serum can also identify a virus isolate in cell culture within 2-3 days. B. Serology. Antibody rise can be detected in paired sera. The CF test is best as long as specificity in addition to accuracy, although the HI test may be used. A 4-fold or greater rise in antibody titer is evidence of mumps infection. A CF test on a single serum sample obtained soon after onset of illness may serve as long as a presumptive diagnosis. S (soluble) antibodies develop within a few days after onset in addition to sometimes reach a high titer be as long as e V (viral) antibodies can be detected. In early convalescence, both S in addition to V antibodies are present at high levels. Subsequently, S antibodies disappear more rap­idly, leaving V antibodies as a marker of previous infection as long as several years. The intradermal injection of inactivated virus results in reappearance of V antibodies in high titer. Neutralizing antibodies also appear during convalescence in addition to can be determined in cell culture. C. Skin Test Antigen: Delayed type hypersensitivity may be noted about 3-4 weeks after onset. The skin test is less reliable than serologic tests to establish evidence of past infection. Immunity Immunity is permanent after a single infection. Only one antigenic type exists. Passive immunity is transferred from mother to offspring; thus it is rare to see mumps in infants under age 6 months. Treatment Gamma globulin is of no value as long as decreasing the incidence of orchitis, even when given immediately after parotitis is first noted.

Epidemiology Mumps occurs throughout the world endemically throughout the year. Outbreaks occur where crowding favors dissemination of the virus. The disease reaches its highest incidence in children age 5-15 years, but epidemics occur in army camps. Although morbidity rates are high, the mortality rate is negligible, even when the nervous system is involved. Humans are the only known reservoir of virus. The virus is transmitted by direct contact, airborne droplets, or fomites contaminated with saliva in addition to , perhaps, urine. The period of communicability is from about 4 days be as long as e to about a week after the onset of symptoms. More intimate contact is necessary as long as the transmission of mumps than as long as measles or varicella. About 30-40% of infections with mumps virus are inapparent. Individuals with subclinical mumps acquire immunity. During the course of inapparent infection, they can serve as sources of infection as long as others. Antibodies to mumps virus are transferred across the placenta in addition to are gradually lost during the first year of life. In urban areas, antibodies are then acquired gradually, so that the 15-year-old group has about the same prevalence of persons with antibodies as the adult group. Antibodies are acquired at the same rate by persons living under favorable in addition to unfavorable socio-economic conditions. Control Mumps is usually a mild childhood disease. A live attenuated vaccine made in chick embryo cell culture is available. It produces a subclinical noncommunicable infection. The vaccine is recommended as long as children over age 1 year in addition to as long as adolescents in addition to adults who have not had mumps parotitis, A single dose of the vaccine given subcutaneously produces detectable antibodies in 95% of vaccinees, in addition to antibody persists as long as at least 8 years. Combination live virus vaccines (measles-mumps-rubella) produce antibodies to each of the vi­ruses in about 95%. In 1967, the year mumps vaccine was licensed, there were about 200,000 mumps cases ( in addition to 900 patients with encephalitis) in the USA. After 10 years of vaccine use, the number of mumps cases in 1977 was about 22,000, with 70 cases of encephalitis.

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PARAINFLUENZA VIRUS INFECTIONS The parainfluenza viruses are paramyxoviruses with morphologic in addition to biologic properties typical of the genus. They grow welt in primary monkey or human epithelial cell culture but poorly or not at all in the embryonated egg. They produce a minimal cytopathic effect in cell culture but are recognized by the hemad-sorption method. Laboratory diagnosis may be made by the HI, CF, in addition to Nt tests. Parainfluenzae virus PIV STRUCTURE

PIV- transmission through droplet dispersion (Courtesy-American Assoc. as long as the Adv. Of Science) Parainfluenza 1 Included here are Sendai virus, also known as the hemagglutinating virus of Japan (HVJ), in addition to hemadsorption virus type 2 (HA-2). Sendai virus may be a causative agent of pneumonia in pigs in addition to newborn infants. Sendai virus is important in somatic cell genetics, where it is used to produce cell fusion. Clinically, the most important member of this group appears to be the widespread HA-2 virus. It is not cytopathogenic as long as monkey kidney cell cultures but is detected in such cultures by the hemadsorption test. It is one of the main agents producing croup in children, but it can also cause coryza, pharyngitis, bronchitis, bronchiolitis, or pneumonia. In adults it produces respiratory symptoms like those of the common cold, with reinfection occurring in persons with antibodies from earlier infections. Natural infection stimulates antibody appearance in nasal secretions in addition to concomitant resistance to reinfection, An experimental killed vaccine induces serum antibodies but does not protect against infection

Preventing Spread H in addition to washing Disinfection of surfaces Gloves, masks, goggles, gowns Isolation, in addition to cohort nursing Immunization Prevention of Disease Active Immunization Formalin inactivated vaccine resulted in enhanced disease Subunit vaccines being studied Prevention of Disease Passive immunization (immunoprophylaxis) Pooled hyperimmune globulin (RespiGam) Monoclonal antibody to F protein- Palivizumab (Synagis)

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