Virus 1 Flashcards
What is a virus
obligate intracellular parasites
Require the cellular machinery of the host cell for replication
A single virus particle =
What is it comprised of?
virion and it is comprised of the viral genome (RNA or DNA) surrounded by a protein coat known as a capsid
How big are viruses
TINY
Viral replication
They attach to a receptor cell (specificity - not every virus can attach to every receptor)
Requires a lot of machinery from the host for cell transcription
Viral replication - drugs
Drugs often are aimed to interrupt the attachment of the virus onto the receptor - they interrupt the packaging process that is needed for replication to occur
Viral transmission - how
Most viruses = entry through breaks in skin, across mucus membranes (resp/GI/urogenital)
Some - bite of insects
Viral transmission - most common route of viral infection
Inhalation of respiratory droplets
Viral transmission - the route of infection depends on what
the site of viral replication within the host
Ex - flu = resp tract = inhalation of droplets
Ex - enterovirsuses = GI = fecal-oral
Route of transmission - Respiratory droplets
Influenza
Measles
Varicella Zoster
Route of transmission - GI fecal/oral
Hepatitis A, Rotavirus, Poliovirus
Route of transmission - Lesion contact
Herpes simplex
Smallpox
Route of transmission - Blood and body fluids
Hep B and C
EBV
CMV
Route of transmission - insect bites
West nile virus
Viral transmission - some viruses are able to survive in the external environment better than others - which?
Enveloped = very fragile and must remain wet Non-enveloped = can withstand harsher environments
Viruses and cancer -
Some viral infections can result in uncontrolled cellular growth causing cells to become transformed
End result of this transformation is frequently cancer
Viruses and cancer - Human papilloma virus
Cervical cancer
Viruses and cancer - EBV
Burkett’s lymphoma
Viruses and cancer - HHV8
Kaposi’s sarcoma
Viruses and cancer - Hep B
Hepatocellular carcinoma
Antiviral immune mechanisms - natural barriers
skin, mucus, gastric acidity, tears, bile
Antiviral immune mechanisms - Nonspecific or innate immune mechanisms
Macrophages, neutrophils, monocytes
Antiviral immune mechanisms - Adaptive immune response
Antibody and T cell responses - natural killer cells, cytotoxic T lymphocytes
Virus - diagnosis
Very difficult!
Reasonable and accurate can be made on clinical presentation (s/s, age)
Virus - diagnosis - definitive diagnosis
Growing the virus in culture
Detecting viral proteins or genome in clinical material (blood, feces, skin scrapings, swabs)
Detecting antibodies in the pt which recognize a specific virus
Antiviral drugs
More antibiotics for bacterial infections than viral
Viral is a lot more of preventative drugs
Antivirals tend to be more selective than broad acting antibiotics - antivirals tend to target only a select group or a specific virus
Viruses causing skin disease - cutaneous manifestations of viral infection (rash/exanthem)
Viral replication in epidermis - HPV, HSV, smallpox
Secondary effect of virus replication elsewhere in body - measles, rubella
Viruses causing skin disease - routes of infection
Primary infection - mucosal contact, breaks in skin
Secondary - viremia (it infects skin following replication)
!Rash may develop as a result of immune response!
Viruses causing skin diseases - childhood exanthems
Chicken pox Measles Rubella Roseola infantum (HHV 6,7) Fifth disease (parvovirus B19)
Herpes Virus - description
Large enveloped viruses
Have the ability to enter a latent phase following primary infection, with potential for later reactivation
HHV 1
Fever blisters, ocular lesions, CNS infections
Think above the waist
1/3 children seropositive by age 5
2/3 adults by age 30
HHV 2
genital and anal lesions, neonatal infections, CNS infections
Think below the waist
seroprevalence 15-20%
HSV 1 and HSV 2 are both transmitted through what
direct contact with virus containing secretions
1 = kissing, sharing saliva
2 = sexual contact, infected mother to child with birth
HSV 1 and HSV 2 pathogenesis
Following inoculation, virus enters and replicates within epithelial cells at site of inoculation
Infection can be asymptomatic or result in lesion
Life long latent infection is typically established in the regional ganglion
HS1 and HS2 - mechanisms that trigger reactivation of latent infection are thought to be
environmental - UV light, fever, stress, trauma
Herpes labialis =
cold sore/fever blister
Herpes labialis - adutls
if primary infection occurs in adulthood, usually asymptomatic
Adults sometimes will develop lesions on the pharynx and tonsils
Herpes labialis - incubation period
thought to vary from 2 to 12 days
clincial disease resolves in 5-10 days
Viral shedding may occur for weeks
Herpes labialis - reactivation is preceded by what
a prodrome of pain, burning, tingling, or itching that generally lasts for 6 hours and is followed by vesicle eruption
Herpes labialis - lesions will ulcerate and crust over in
3 to 4 days
Herpetic whitlow =
HSV infection of the fingers and nails, following inoculation of secretions into small cuts
Usually occurs in children, individuals with genital herpes, and physicians, dentists and healthcare providers who treat herpes patients
Herpes gladiatorum =
An infection of the body (skin) - Most commonly observed in wrestlers and rugby players
HSV 1 and HSV 2 - diagnosis
1 -Can be confirmed by sampling material at the base of a lesion (Tzanck smear)
And demonstrating the presence of multinucleated giantt cells or Cowdry type A inclusions
2 -cultivation of the virus in tissue culture and observation of characteristic cytopathic effect (CPE)
3 -PCR techniques
HSV 1 and HSV 2 - Treatment
Acyclovir and related compounds
Modest benefit in tx of herpes labialis - can do proph
Topical therapy of eye infections with acyclocir
HSV 1 and HSV 2 - prevention and control - health care workers with HSV on figners and hands
restricted from contact with patients until lesions are healed
HSV 1 and HSV 2 - prevention and control - personnel with orofacial lesions
should be counseled to cover their lesions and not touch lesions with their hands
Case by case analysis for those with orofacial and deciding their exposure to high risk patients that are immuno compromised
HHV 3
Varicella zoster virus causes two diseases
Varicella (chicken pox)
Zoster (shingles)
HHV 3 - primary vs. latent
Chicken pox develops after primary infection
Shingles results from reactivation of latent virus
HHV 3 - Thought to be transmitted primarily though
respiratory droplets
Extremely contagious!
HHV 3 - transmission
virus can be isolated from skin lesions but is difficult to isolate from resp tract
VZV can be transmitted to others for 1-3 days prior to the onset of the rash
HHV 3 - pathogenesis
Virus becomes latent in sensory ganglia (usually trigeminal and dorsal root ganglion)
Lesions have characteristic dermatomal clustering
With reactivation, virus replicates and is released along neuronal pathway
Chicken pox - description
No evidence of prodrome in children, adults may experience 1/2 days of malaise and fever
Fever and rash appear simultaneously on trunk and head rather than extremetites
Lesions appear in crops
Within 12-24 hrs will crust and scab over
Shingles - description
lesions occur unilaterally along dermatome supplied b y adorsal route or CN sensory ganglion
Severe pain typically precedes the eruption
Postherpetic neuralgia may persist
HHV 3 - treatment
Several compounds including acyclovair can work if administered within 24 hrs of onset - reduce number of lesions and duration of fever (not usually used in kids)
HHV 3 - prevention/control
live attenuated vaccine
given to children at 12-18 months of age and is also recommended in adults over 60
HHV 3 - prevention/control - healthcare workers who develop it should
be excluded from work until all lesions have crusted over and dried
exclude from duty personnel who have been exposed to it and are not known to be immune
HHV 3 - work restrictions should be in effect from
10 th day after first exposure to the 21st day after last exposure
