Viruses Flashcards
Measles and Mumps structure
enveloped negative strand RNA viruses
Rubella structure
Enveloped positive strand RNA virus
Erythema infectiosum infectious agent
Caused by Parvovirus B19; also called fifth disease
Erythema infectiosum modes of transmission
respiratory tract secretions, percutaneous exposure to blood or blood products, vertical transmission from mother to fetus
Erythema Infectiosum incubation period and infectious time
1-2weeks from exposure to onset of rash; most infectious before onset of rash
Parvovirus B19 infectious cycles
bi-phasic: lytic, infectious phase; then non-infectious, immunologic phase where IgG neutralizes circulating virus
Parvovirus B19 symptoms
symptoms are immune mediated; cytokines produce prodromal flu-like symptoms followed by cell-mediated response causing a rash
Measles type
Morbillivirus of Paramyxoviridae family; differentiated from other paramyx viruses receptor usage (primary MV receptor are CD46, SLAM, Nectin 4; has H Protein) and forms intracellular inclusion bodies (distinctive feature of cytopathology)
Measles healthcare policy and vaccination
report to health department cases of measles; vaccine can be given within 72 hours of exposure
Measles Clinical Defniition
Generalized rash lating more than 3 days and temperature greater than 101 and cough, coryza, conjunctivitis.
Basis of Measles rash
Morbiliform rash due to cytotoxic T cells attacking measles virus infected vascular endothelial cells in the skin
Measles mode of transmission
highly contagious and spread via respiratory droplets
Primary cause of death in Measles
bacterial pneumonia due to measles induced immunosuppression
Symptoms of Measles
start 10-14 days post exposure; prodrome of fever, cough, conjunctivitis, coryza, with high fever, photophobia, followed by appearance of maculopapular rash
Rash coincides with what in Measles
coincides with a strong cell-mediated immune response and virus clearance
Koplik spots
bluish-white abruptions found in the mouth, often preceding rash; pathognomonic for measles
Measles complications
immune suppression probably due to infection of monocytes and other immune effector cell; acute disseminated encephalomyelitis, post infectious encephalomyelitis, measles inclusion body encephalitis, subacute sclerosing panencephalitis
Measles vaccine
antigenic ally stable monotypic virus, so works every year; live attenuated measles virus provides life long immunity
Viruses that cause harm to fetus if infection during pregnancy
Parvo-B19 and Rubella
Rubella symptoms
mild disease characterized by a low-grade fever, occasional conjunctivitis and sore throat, LAD, and a morbilliform rash that starts on the face and spreads to the rest of the body
Rubella transmission and replication
Transmitted via aerosols; repicaltion occurs in URT mucosa and the nasopharyngeal lymph nodes; viremia develops, rash develops after 16-21 days; virus shedding continues after the rash disappears
Rubella birth defects
cause mental retardation, motor disabilities, hearing loss, congenital heart disease, and cataracts; more serious the during 1st and 2nd trimester
Parvovirus B19 affects on pregnancy
hydrops fetalis, intrauterine growth retardation, pleural and pericardial effusions, and death
Parvovirus B19 complications
immunodeficiency (chronic erythroid hypoplasa with severe anemia) and chronic hemolytic anemia (esp in sickle cell)
Four major Enteroviruses
Coxsackievirus, Echovirus, Enterovirus, Poliovirus
Enterovirus differentiation from Rhinovirus
acid stabile, less stringent growth requirements, and humans are only known reservoir
Enterovirus spread and replication
spread by oral-fecal route or by aerosol contamination of fomites; repicale in lymphoid tissue of URT and the gut, followed by viremia; usually asymptomatic
Coxsackie A16 causes what
Hand, Foot, and Mouth Disease
Hand foot and mouth symptoms
ulcerative lesions on the tonsils and uvula (herpangina), fever, sore throat, HA, ab pain, vesicular lesions on hands and feet
Hand foot and mouth treatment
Disease is self limiting and requires only symptomatic management but it is highly contagious
Hand foot and mouth virus isolation
can be caused by Coxsackievirus A16, A6 and eneterovirus 71; can be isolated from lesions and from feces
Enterovirus control
no vaccines available for any other enterovirus than polio; most infections and self limiting and are often asymptomatic
Roseola infantum symptoms
young child, high fever, nasal congestion and loose stools for under one week, followed by a rosy-pink rash on torso, arms, and neck that is not pruitus and goes away after a few days
Age range for Rosela infections
6mo-4years; most common exanthem before age 2; nearly everyone has been exposed by age 3-4
Complications of HHV-6/7 infection
reactivation in brain, lungs, heart, kidney, and GI tract; associated with immunosuppression (stem cell transplant); reactivation in brain can cause cognitive dysfunction, permanent disability and death
Mumps pathogenesis
infection in mucosal epithelium of nasopharynx and URT; incubation of ~18 days; virus si shed in saliva 6 days before onset of clinical disease
Mumps symptoms
swelling and inflammation of parotid gland; no rash
Mumps complication
virus replication in CNS causing aseptic meningitis or infection of cochlea leading to deafness; symptomatic gonadal involvement causing enlargement of the testes which can cause tissue damage and sterility
Viral cause of Roseola
HHV-6/7
HPV structure
circular ds-DNA, non-enveloped icosahedral capsid virus
HPV pathogenesis
many strains; infect epithelia of skin and mucous membranes, causing warts in different locations and of different morphology depending on strain of virus; warts are benign neoplasms that can progress to malignancy
Permissive cells
infectious virus progeny are produced (lytic replication)
Non-permissive cells
genome is replicated, but no virus particles are produced; late (structural) proteins are not expressed, no capsize proteins are made; this leads to cell transformation
Morphogenesis of a wart
HPV latently infects basal epithelial cell; as the cell replicates and proliferates, there is high level episomal replication of the virus as well; once a terminally differentiated keratinocyte, virus assembly and release occurs with HPV shedding
Benign tumors of HPV
non-permissive, persistently infected cells that have a genome that is circular, full-length and extra-chromosomal
Malignant tumors of HPV
a partial genome that has lost the E2 gene is integrated into the host DNA, resulting in retention of E6 and E7 and disregulation of E2 mediated transcriptional control
E6 function
degradation of p53
E7 function
inactivates Rb protein
HPV diagnosis
clinical appearance, genotyping is possible; HPV cannot be routinely grown in the lab
HPV treatment
most warts spontaneously regress; can be removed surgically, cryosurgical, or through corrosives; drug treatment is also available; recurrences are common due to survival of infected cells in basal layer
HPV Vaccine
virus like particles from HPV 6, 11, 16, 18 made in yeast that consist of the L1 capsid protein from each that self assembles into pseudocapsids
Pox viral structure
large complex structure that is enveloped; ds linear DNA genome
Pox virus replication
all replication takes place within cytoplasm; virus penetrates the cells and loses its outer membrane, then as it releases viral DNA makes its own enzymes needed for replication, replicates within the cytoplasm and the virus is released from the cell by cell disruption or exocytosis
Small pox symtoms
systemic disease with generalized rash that had high fatality; fever and rash precede the pustules that are created by small vessel cutaneous hemorrhage
Small pox virus infective mechanism
inhalation or transmission by scabs, replication in URT, lymphatics (macrophages) transmit virus to lymph nodes where a viremia occurs that is associated with hemorrhage of small vessels in dermis and infection of other organs; viremia is associated with the appearance of pustules
Mortality in small pox
death is due to toxic effects on vascular endothelium
Childhood molluscum contagiosum
lesions on the face, trunk, and limbs that spread from skin to skin
Young adult molluscum contagiosum
mostly lower abdomen lesions, sexually-transmitted
Molluscum contagious disease course and diagnosis
lesions disappear in 2-12 months; diagnosis by appearance, confirmed by presence of cytoplasmic inclusions in keratinocytes of the affected area
Small pox vaccine
live vaccine, localized lesion that heals in two weeks, wanes after 3 years, gone after 20 years
Keys to small pox eradication
humans are only reservoir; no healthy carriers existed; no sub-clinical infections; effective vaccine was available
Adverse small pox vaccine reactions
Could not be given to: pregnant or breast feeding women, immunodeficient, atopic dermatitis pts, under 18yo in non-emergency situation, people with heart disease; generalized vaccinia, inadvertent inoculation, erythema multiforme; adverse reactions are common
Life-threatening small pox vaccine complications
progressive vaccinia and eczema vaccinatum
Herpes Viral Structure
linear, dsDNA genome, icosahedral capsid, enveloped, dozen glycoproteins; DNA is replicated and viruses are assembled in the nucleus
Lytic Cycle of Herpes Virus
Immediately upon entry into the cell the virus makes transcription factors, then it replicates, then makes structural proteins and is exocytosed from the host cell to infect other cells
Herpes Neuronal Replication
peripheral sensory neurons directly take up the progeny of epithelial replication, these progeny viruses as they replicate are trans synaptically transported in the retrograde direction
Herpes Latency
nor virus particles are produced, entire genome is maintained extrachromosomally, and few viral genes are expressed
Location of HSV-1 latency
Trigeminal Nerve
Location of HSV-2 latency
sacral and lumbar nerves
Location of VZV latency
Dorsal Root
Herpes LAT
Latency associated transcript; it prevents lytic replication, prevents apoptosis of infected neuron and evades immune surveillance (CD8), allowing the virus to enter latency
HSV-1 Disease locations
skin (especially around mouth), eyes, encephalitis
HSV-2 Disease locations
Urogenital and Meningitis
HSV pathogenesis
spread via secretions through breaks in skin or mucosa; replicates in epithelial cells at site of infection then spread to lymph nodes; primary infection is often unapparent
HSV Diagnosis
clinical features, serology for primary infections; PCR, Tzanck smear
VZV Pathogenesis
primary infection causes chickenpox; spread by aerosol, causing itchy rash starting on scalp and trunk
VZV Reactivation
reactivation causes shingles, sudden onset of pain and rash along thoracic dermatome or forehead with a rash lasting 2-4 weeks, thought the pain lasts much longer
VZV diagnosis
clinical appearance; Tzanck smear
