Coordinated AP-assisted Medium Synchronization Recovery
This document discusses the concept of medium synchronization recovery leveraging multi-AP coordination for multi-link devices in IEEE 802.11 networks. It addresses the challenges and solutions related to AP-assisted medium synchronization recovery in wireless communication systems.
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Enveloped RNA Viruses Paramyxoviruses
Measles, mumps, parainfluenza viruses, respiratory syncytial virus, human metapneumovirus
Table 1 Envelope Spikes of Paramyxoviruses Virus Measles virus Mumps virus2 Respiratory syncytial virus Parainfluenza virus2 Hemagglutinin Neuraminidase Fusion Protein1 + + + + + + + + + 1The measles and mumps fusion proteins are hemolysins also. 2In mumps and parainfluenza viruses, the hemagglutinin and neuraminidase are on the same spike and the fusion protein is on a different spike.
Paramyxoviridae Glycoproteins - do not form such prominent spikes as on influenza virus: HN - haemagglutinin + neuraminidase activities; Measles - referred to as H protein - no neuraminidase activity; RSV - G protein - neither activity. F - consists of 2 disulphide- linked subunits (F1 + F2) - responsible for cell fusion + haemolytic function. Other proteins: The M (matrix) protein lines the inner surface of the envelope. NP - nucleoprotein. L and P - polymerase activity
Paramyxovirus structure Paramyxovirus electron micrograph
Paramyxoviruses Envelope has HN and specialized F spikes that initiate cell-to-cell fusion. Fusion with neighboring cells syncytium or multinucleate giant cells form 7
Insert figure 25.5 Effects of paramyxoviruses 8
Measles: general One of the five classical childhood exanthems (eruptive diseases) rubella (togavirus) roseola (HHV 6) fifth disease (parvovirus, B19, erythema infectiosum) chickenpox (herpes zoster) Host range limited to humans, one serotype
Measles Caused by Morbillivirus Also known as red measles and rubeola Different from German measles Very contagious; transmitted by respiratory aerosols Humans are the only reservoir. 11
Measles pathogenesis Mechanisms of spread of the measles virus within the body and the pathogenesis of measles. CMI, Cell-mediated immunity; CNS, central nervous system.
Measles time course Time course of measles virus infection. Characteristic prodrome symptoms are cough, conjunctivitis, coryza, and photophobia (CCC and P), followed by the appearance of Koplik's spots and rash. SSPE, Subacute sclerosing panencephalitis.
Measles induced syncytia Formation of giant cells (syncytia) in measles pneumonia. Notice the eosinophilic inclusions in both the cytoplasm and nuclei.
Kopliks spots Koplik's spots in the mouth and exanthem. Koplik's spots usually precede the measles rash and may be seen for the first day or two after the rash appears.
Measles Symptoms start about 10 days after exposure Average 10 days from exposure to onset of fever Average 14 days from exposure to onset of rash Other symptoms and complications Ear infection Pneumonia CNS/ brain infection (as SSPE, subacute sclerosing panencephalitis) Complications may be lethal More serious in infants and adults, less in children and teens Vaccine Measles (Paramyxoviridae), mumps (Paramyxoviridae), rubella (Togaviridae, + sense) (MMR) vaccine is a live vaccine Has been very effective in limiting spread Links of vaccine to autism have been proposed but not shown
Subacute-sclerosing panencephalitis (SSPE) Most serious complication is subacute sclerosing panencephalitis (SSPE), a progressive neurological degeneration of the cerebral cortex, white matter and brain stem. Neural manifestation of measles virus Defective form spreading through the brain by cell fusion and destroys cells Specific mutations result in virus that is more fit in neural cells Usually occurs 6-12 years after measles infection More rarely associated with live measles vaccine Infection rate 1 per million; higher in males & rural Mortality high leads to coma and death in months or year
Mumps pathogenesis Mechanism of spread of mumps virus within the body.
Mumps time course Time course of mumps virus infection.
Mumps symptoms Child with parotitis
Mumps Epidemic parotitis; self-limited, associated with painful swelling of parotid salivary glands Humans are the only reservoir. 40% of infections are subclinical; long-term immunity. Incubation 2-3 weeks fever, muscle pain and malaise, classic swelling of one or both cheeks Usually uncomplicated invasion of other organs; in 20-30% of infected adult males, epididymis and testes become infected; sterility is rare Symptomatic treatment Live attenuated vaccine MMR 23
Laboratory Diagnosis The diagnosis of mumps is usually made clinically, but laboratory tests are available for confirmation. The virus can be isolated in cell culture from saliva, spinal fluid, or urine. In addition, a fourfold rise in antibody titer in either the hemagglutination inhibition or the CF test is diagnostic. A single CF test that assays both the S and the V (viral) antigens can also be used. Because antibody to S antigen appears early and is short- lived, it indicates current infection. If only V antibody is found, the patient has had mumps in the past. A mumps skin test based on delayed hypersensitivity can be used to detect previous infection, but serologic tests are preferred. The mumps skin test is widely used to determine whether a patient's cell-mediated immunity is competent. 24
In the late 1980s, outbreaks of mumps occurred in both immunized and unimmunized people. This led to the recommendation in 1989 that a second course of MMR (measles, mumps, rubella) vaccine be administered. The incidence of mumps fell and outbreaks did not occur until 2006 when 6584 cases occurred, primarily in college-age individuals who, surprisingly, had received two doses of the vaccine. Waning immunity after the second dose and immunization with a different genotype from the genotype that caused the outbreak are suggested explanations. 25
Parainfluenza Virus ssRNA virus enveloped, pleomorphic morphology 5 serotypes: 1, 2, 3, 4a and 4b No common group antigen Closely related to Mumps virus
Parainfluenza viruses Four serotypes, host range limited to humans, Respiratory transmission Infections limited to respiratory tract, generally non-systemic and viremia rare Causes cold-like symptoms, bronchitis and croup (laryngotraheobroncitis) (serotypes 1 and 2), Bronchiolitis, . Infections of children common Diagnosis: Detection of Antigen - from nasopharyngeal aspirates and throat washings. Virus culture Syncytia formation Hemadsorption Hemagglutination inhibition rtPCR Serology - a retrospective diagnosis may be made by serology. CFT most widely used Immunity following infection short-lived. Individuals subject to re- infection
Management No specific antiviral chemotherapy available. Severe cases of croup should be admitted to hospital and placed in oxygen tents. No vaccine is available.
Respiratory Syncytial Virus (RSV) ssRNA eveloped virus. belong to the genus Pneumovirus of the Paramyxovirus family. Considerable strain variation exists, may be classified into subgroups A and B by monoclonal sera. Both subgroups circulate in the community at any one time. Causes a sizable epidemic each year.
Clinical Manifestations Most common cause of severe lower respiratory tract disease in infants, responsible for 50-90% of Bronchiolitis and 5-40% of Bronchopneumonia Other manifestations include croup (10% of all cases). Infants at Risk of Severe Infection 1. Infants with congenital heart disease 2. Infants with underlying pulmonary disease 3. Immunocompromized infants In older children and adults, the symptoms are much milder: it may cause a corza-like illness or bronchitis.
Respiratory syncytial virus Widespread: 75% of infants seropositive by 1 year of age Host range limited to humans; single serotype Respiratory transmission Highly contagious; contagion period precedes symptoms and may occur in absence of symptoms Localized infections of respiratory tract, no viremia and no systemic infections Poor immunity Reinfection occurs throughout life Maternal antibody does not prevent infection Diagnosis; Detection of Antigen - a rapid diagnosis can be made by the detection of RSV antigen from nasopharyngeal aspirates. A rapid diagnosis is important because of the availability of therapy Virus Isolation - virus may be readily isolated from nasopharyngeal aspirates. However, this will take several days. rtPCR, immunofluorescence, enzyme immunoassay, Serology; Serology - a retrospective diagnosis may be made by serology. CFT most widely used.
Treatment and Prevention Treatment Ribavarin reduces severity of symptoms in immunocomprimized patients .Aerosolised ribavirin can be used for infants with severe infection, and for those at risk of severe disease No vaccine; improper vaccination increases severity of disease Passive vaccination for high risk infants Palivizumab: anti-F monoclonal antibodyRSV immunoglobulin can be used to protect infants at risk of severe RSV disease.
Human metapneumovirus Respiratory transmission Disease: asymptomatic, common cold, bronchiolotis, pheumonia Accounts for 15% of common colds in children Diagnosis by rtPCR
Paramyxoviridae Paramyxovirinae Hendra and Nipah Viruses Zoonotic viral infections
Reservoir Flying foxes (fruit bats) Carry the virus Are not affected Virus found in Urine Partially eaten fruit Migratory
