Paramyxoviruses, Mumps, RSV, Parainfluenza, Measles, Influenza
Paramyxoviruses
Dentistry 2025
Single-stranded, negative-sense, linear, non-segmented RNA virus.
All members are antigenically stable.
Most contain 6 structural proteins:
3 proteins complexed with RNA
Nucleoprotein → forms the nucleocapsid
P & L → involved in polymerase activity
3 proteins participate in the formation of viral envelope
M protein → matrix protein → important in assembly.
Glycoproteins:
HN or G → for attachment
F (fusion) → for membrane fusion & hemolysin activity
3 spikes in the envelope:
Hemagglutinin
Neuraminidase
Fusion protein → causes cell to cell fusion → Giant cell formation
Paramyxoviridae Genera Members
Respirovirus
Parainfluenza 1,3
Rubulavirus
Mumps
Parainfluenza 2,4a,4b
Morbillivirus
Measles
Henipavirus
Hendra, Nipah
Pneumovirinae
Pneumovirus
RSV
Metapneumovirus
Human metapneumovirus
Mumps Virus
Single serotype.
Neutralizing antibodies against the hemagglutinin.
Humans – natural hosts.
MOT: via droplets.
Mumps/ Viral parotitis:
An acute contagious disease involving the salivary glands.
Characterized by non-suppurative enlargement of one or both salivary glands.
Endemic worldwide.
Highest incidence → children 5-9 y/o
MOT:
Direct contact
Airborne droplets
Fomites
Primary replication → URT epithelial cells → viremia → salivary glands & other areas (meninges, testes, pancreas, ovaries, breast).
Involvement of the parotid glands is not an obligatory step in the infectious process.
IP: 2-4 wks (14-18 days).
Virus shedding: 3 days before up to 9 days after onset of gland swelling.
Clinical findings:
Prodromal period → anorexia & malaise.
Enlargement of parotid glands & other salivary glands with associated pain.
Complications of Mumps:
Orchitis
When bilateral → sterility.
Post-pubertal males have fibrous tunica albuginea which resists expansion → pressure necrosis of the spermatocytes.
Meningitis
Benign, self-limiting.
Mumps orchitis:
Testicular swelling
Edema, mononuclear cell infiltration, and focal hemorrhages.
Parenchymal swelling → compromise blood supply → areas of infarction.
Diagnosis:
Isolation & identification of the virus
Culture → monkey kidney cells
Immunofluorescence
CPE
Hemadsorption inhibition
Nucleic acid detection → PCR
Serology → ELISA or HI
Treatment & Prevention
No specific treatment.
Immunization → MMR → 2 doses.
Respiratory Syncytial Virus (RSV)
Replication initially occur in the epithelial cells of the nasopharynx → LRT → bronchiolitis & pneumonia.
Most common cause of bronchiolitis & pneumonia in infants (6wks-6 months; peak = 2 months).
IP: 3-5 days.
Virus shedding:
Infants & young children → 1-3 weeks
Adults → 1-2 days
Severe infection in infants → immunopathogenic mechanism → maternal antibodies passed to the infant may react to the virus → damage cell in the respiratory tract.
In older children & adults → mild infections like common colds.
Account for 1/3 of respiratory infections in bone marrow transplant patients.
Important cause of otitis media in infants especially during wintertime.
Immunity is incomplete → recurrent infections.
Laboratory diagnosis:
Antigen detection – immunofluorescence or ELISA
Culture – Human heteroploid cell lines (HeLa cells & HEp-2 cells)
Nucleic acid detection – PCR
Serology – immunofluorescence, ELISA or Nt tests
Treatment & Prevention:
Supportive care → removal of secretions, administration of oxygen
Antiviral drug → Ribavirin → aerosol for 3-6 days
Vaccine:
Immune globulin with high titer antibodies → marginal benefit
Humanized antiviral monoclonal antibodies
Parainfluenza Viruses
4 serotypes.
Most common cause of croup (acute laryngotracheobronchitis) in children under 5 yrs of age (Parainfluenza 1 & 2).
Manifestation: harsh cough & hoarseness.
Measles Virus (Rubeola Virus)
Measles → an acute, highly infectious disease characterized by fever, respiratory symptoms & maculopapular rash.
Key immunologic features of measles:
Highly contagious
Only one serotype
No animal reservoir
Inapparent infections rare
Infections confers lifelong immunity
Humans are the only natural host for measles virus.
Entry into the RT → multiply → regional LN → multiplication → primary viremia → RES → multiply → secondary viremia → skin, RT, conjunctivae → replication.
Entire events occur during the IP (8-12 days).
Virus is present in tears, nasal & throat secretions, urine & blood during the prodromal phase (2-4 days).
Day 14 → maculopapular rash appear as circulating antibodies become detectable → viremia disappears & fever decreases.
Rash → due to cytotoxic T cell attacking the measles virus infected vascular endothelial cells in the skin.
In patients with defective CMI → no rash develops.
CNS is commonly involved in measles → encephalitis → may be due to autoimmune reaction.
Rare late sequelae → SSPE (subacute sclerosing panencephalitis) → develop years after initial measles infection & due to virus that remains in the body after acute infection.
Clinical findings
IP 8-12 days → 7- 11 days illness
Prodromal phase (2-4 days)
3 C’s → cough, coryza, conjunctivitis
fever
Koplik spots → “grains of salt” → appear 2 days before the rash
Eruptive phase (5-8 days) → maculopapular rash starting from the head → chest → trunk → extremities → 5-10 days → desquamation
In partially immune individuals → prolonged IP, diminished prodromal manifestations, (-) Koplik spots, mild rash
Complications:
Otitis media → most common (5-9%)
Secondary bacterial pneumonia → most common life-threatening complication (10% & 20-80%)
Giant cell pneumonia → in CMI deficient individuals
CNS complications
Acute encephalitis
Postinfectious encephalomyelitis (acute disseminated encephalomyelitis) → neurological sequelae
SSPE → progressive mental deterioration, involuntary movements, muscular rigidity & coma
Immunity
Infection confers lifelong immunity
Cellular immunity → essential for recovery & protection
Immunoglobulin def. → recover from measles & resists reinfection
CMI def → do very poorly
Treatment, prevention & control
Vitamin A treatment → decrease morbidity & mortality
Vaccine → MMR or MMRV
Contraindications to vaccine:
pregnancy
allergy to eggs or neomycin
immune compromise
recent immunoglobulin administration
Comparison of Rubeola and Rubella:
Property | Rubeola (Measles) | Rubella (German Measles)
Common name | Measles | German measles
Etiology | Paramyxovirus | Togavirus
MOT | Inhalation of droplets | Inhalation; transplacental
Enanthem | Koplik’s spots | Forschemer’s spots
Fever | + | +
3 C’s (coryza, cough, conjunctivitis) | + + + (with photophobia) | + (mild) - + (w/o photophobia)
Exanthem | Maculopapular with desquamation | Maculopapular; pruritic w/o desquamation
Brawny desquamation | + | -
Lymphadenopathy | - | +
Arthralgia | - | +
Congenital infection | - | +
Vaccine | + | +
Hendra Virus & Nipah Virus Infections
Zoonotic
Natural hosts for both viruses → fruit bats
Reasons for emergence:
Ecologic changes (land use)
Animal husbandry practices
1998-1999 → severe encephalitis due to Nipah virus in Malaysia → transmitted from pigs to humans
Hendra virus – an equine virus → caused human fatalities in Australia
Classified as Biosafety Level 4 pathogens
Influenza
Commonly called “the flu”.
A contagious respiratory illness caused by influenza viruses (Family Orthomyxoviridae).
Infection with influenza viruses can result in illness ranging from mild to severe with life-threatening complications.
1918 Spanish flu pandemic: Estimated 20 to 50 million deaths worldwide.
Influenza is Highly Contagious
Virus spread via water droplets, and small particle aerosols when coughing or sneezing
Virus enters the body through nose, mouth and eye
Viral Titers Peak Early:
Peak of viral replication and rapid onset of symptoms occur within 0-5 days.
Influenza - Clinical Signs and Symptoms
Incubation period for influenza is 1-4 days, with an average of 2 days
Adults: infectious from the day before symptoms begin through approximately 5 days after onset
Children: infectious for >10 days, and young children can shed virus for <6 days before their illness onset
Immunocompromised persons can shed virus for weeks or months
Resolves after a limited number of days for the majority of persons, although cough and malaise can persist for >2 weeks
Young children can have initial symptoms mimicking bacterial sepsis with high fevers; <20% of children hospitalized with influenza can have febrile seizures
Influenza infection has also been associated with:
Encephalopathy
Transverse myelitis
Reye syndrome
Myositis
Myocarditis
Pericarditis
Influenza - Hospitalization & Deaths
Populations at risk for complications, hospitalizations, & deaths:
>65 years old & young children
Persons of any age with certain underlying health conditions:
Cardiovascular and pulmonary (including asthma), metabolic e.g. DM, Hgbpathies, immunosuppression
Receiving long term ASA
Seasonal
In colder countries, flu is largely seen during colder months, and they vaccinate prior to this season (e.g. October).
In tropical countries, flu is seen all year round.
Influenza virus types
Three: Influenza A, B, and C
Influenza types A or B viruses cause epidemics; influenza A may cause pandemics
Getting a flu shot can prevent illness from types A and B influenza but not from type C
Influenza type C causes mild respiratory illness; not thought to cause epidemics
Influenza A virus
Contains surface proteins HA and NA. The influenza A virus genome includes:
PB2
PB1
PA
HA
NP
NA
M1
M2
NS1
NS2
RNP
Influenza Replication
The entire Influenza A virus genome is 13,588 bases long and is contained on eight RNA segments that code for 11 proteins
RNA synthesis takes place in the cell nucleus, while the synthesis of proteins takes place in the cytoplasm
Viral proteins are assembled into virions and leave the nucleus, migrating towards the cell membrane.
Host cell membrane has patches of viral transmembrane proteins (HA, NA, and M2) and an underlying layer of the M1 protein, which assist the assembled virions to budding through the membrane
Influenza A virus divided into subtypes based on HA and N proteins on surface
18 HA, 11 N
Nomenclature based on: site of origin, isolate number, year of isolation, subtype
Example: influenzaA/Johannesburg/33/94(H3N2)
Drift or shift
“Antigenic drift" - small changes in the virus that happen continually (influenza A and B)
“Antigenic shift” - abrupt, major change in the influenza A viruses, resulting in new H &/or new H and N proteins that infect humans (influenza A only)
Influenza subtypes in humans
Current subtypes of influenza A viruses found in people are A(H1N1) and A(H3N2)
Influenza B virus is not divided into subtypes
Influenza A(H1N1), A(H3N2), and influenza B strains are included in each year's influenza vaccine
Protection is serotype specific
Recorded human pandemic influenzas since 1885 (early sub-types inferred)
Includes: Russian influenza, Spanish influenza, Asian influenza, Hong Kong influenza, and Swine Flu pandemic.
Most recent Flu Pandemic: novel A(H1N1)
Quadruple reassortant: 2 NA bird flu genes, 1 swine flu, human flu
Thrives in lower respiratory tract
More contagious
Has now become seasonal flu
Resistant to amantadine, rimantadine
Avian Influenza
Many subtypes of influenza A virus subtype of avian influenza
Low pathogenicity avian influenza (LPAI)
Highly pathogenic avian influenza (HPAI)
First recognized in Italy in 1878
Extremely contagious in birds
Rapidly fatal, high mortality (almost 100% in a few days)
Documented in humans: H5N1, H7N3, H7N7, H7N9, and H9N2, H10N8
Treatment of Influenza
Antiviral Medications:
Antiviral drugs: adamantanes: amantadine, rimantadine; neuraminidase inhibitors: zanamivir, oseltamivir
Antiviral treatment lasts for 5 days and must be started within the first 2 days of illness.
Flu vaccination
Inactivated vaccines: the whole virus vaccine, split virus vaccine (disrupted by detergent), and subunit vaccine (H and N purified). Some formulations include adjuvants
Live, attenuated influenza vaccines have been based on a temperature-sensitive variant vaccine virus strains that replicate well in the nasopharynx but poorly in the lower respiratory tract
Vaccination should be given once a year preferably from February to June
The Southern Hemisphere vaccine which is made available starting February of each year is recommended to cover the expected increase in influenza activity from June to November. “Try not to be a man of success, but rather try to become a man of value” - Albert Einstein