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220 Cards in this Set

  • Front
  • Back
structure of a virus as compared to a bacteria
small genome with protective covering
OBLIGATE INTRACELLULAR PARASITES
what is the only thing viruses know how to do
get inside susceptible cell and reproduce
viruses associated with one genus of animals tend to be able to infect that one genus and sometimes only one species only
HOST RANGE
even within a single genus and species, a single kind of virus can infect a limited number of cell types
CELL RANGE
Viral genomes are made of
DNA or RNA (never both)

can be ss or ds
a single haploid virus particle
virion

BUT

retroviruses are not haploid
ds (MOST) or ss (Parvovirus)

genome is either closed circle or a single linear piece
DNA viruses
ds (Reovirus) or ss (MOST)

genome is either single linear piece or segmented into several linear pieces (influenza)
RNA viruses
surrounds the viral genome

protects genome from environment

****determines the infectivity of the virus***
Viral Capsid

(ALL VIRUSES HAVE)
made of protein molecules that are specified by the viral genome
can be several different proteins that aggregate to form building blocks (CAPSOMERES) which in turn coalesce to form a hollow sphere around the viral genome
Viral Capsid
component of the viral capsid that is a single, folded polypeptide chain
subunit/protein subunit
component of the viral capsid that is a collection of one or more nonidentical (or identical) subunits which form a building block for a larger unit
Structure unit/protomer
component of the viral capsid that is a set of structure units forming a sub-assembley of the capsid (ie pentamer, hexamer)
Assembly unit
component of the viral capsid that are "lumps or clusters" on the capsid surface which are visible in the electron mircoscope (CAPSOMERE)
Morphological Unit
type of capsid symmetry that is a spherical hollow shell made of 2 kinds of assembly units of different shapes

MINIMUM: 12, five-sided, Pentamers (NECCESSARY TO FORM A SPHERE

CAN HAVE: variable number of six-sided, hexamers (DETERMINES THE SIZE OF THE COMPLETED CAPSID
Icosahedral
in icosahedral symmetry, the spaces betwen the pentamers which expand the size are
Hexamers
triangles used as subunits to make the hexamers and pentamers in icosahedral symmetry
quasi-equilvalence
larger than assembly units and seen morphologically
CAPSOMERES
proteins that raidate out from the pentamers

**determines the infectivity (esp the knob on the end)
Spike proteins
type of capsid symmetery in which identical capsomeres aggregate to form a helical ribbon-like structure surrounding the viral genome
HELICAL


ALL RNA VIRUSES HAVE!
which virus has a combo of helical and icosahedral symmetry
RABIES
in some viruses, located exterior to the capsid,

derived from a lipid-bilayer membrane of the host cell (ie nuclear mem, cytoplasmic mem)

Unique, virally speicified glycoproteins (PEPLOMERS) inserted into them
ENVELOPE
lipid bilayer is derived from
HOST
glycoproteins are derived from
virus
what are essential to viral infecitivity
Envelope and Peplomers
glycoproteins inserted into the membranes comprising the viral envelope

determines and is essential for viral infectivity
PEPLOMERS
what determines a virus' ability to survive in an hostile environment BUT does not determine its pathogencity
Envelope vs non-envelope

Env.--> easier to inactivate outside of the body with disinfectants
if remove a viral envelope what is left
nucleo-capsid
intermediate proteins that are positioned between the viral envelope and the capsid

some are transmem proteins

some are held to the inner leaflet of the envelope by hydrophobic bonds
MATRIX PROTEINS
connect the nucleocapsid to the mem envelope

perform a crucial function during the assemble of progeny virions during replication
MATRIX Proteins
what can induce an immune response (cell mediated) (esp when glycoproteins adhere to the cell membrane)
spike proteins
what is best viral example of complex symmetery
vaccinia virus
used to immunize against small pox

large dumbbell-shpaed genome

genome is surounded by several layers of protein with no discernible capsid symmetry

protein is surrounded by sveral layers of lipid
vaccinia virus

POX IN A BOX
what is the largest animal virus
pox viruses
DNA virus that replicates in the cytoplasm of the host

(DNA viruses usually replicate in the nucleus)
Pox viruses
steps of viral replication
1. attachment or adsorbtion
2. viral penetration
3. uncoating
4. eclipse (synthesis of genome and viral proteins)
5. assembly of progeny virions
6. release of non-enveloped / enveloped progeny virions
cell attachment sites distributed over the viral surface



(ATTACHMENT CAN BE BLOCKED BY SPECIFIC ABS)
capsid (non-envel viruses)
envelope peplomers (envel viruses)
suceptible cells have what on their surfaces
viral receptors
process by which the virus enters the cytoplasm of a susceptible cell
penetration
penentration can occur by what 3 mechanisms
Translocation (non-envel.)
Fusion (enveloped)
Viropexis (receptor-mediated endocytosis)--->MOST COMMON (both non-envel and envel)
pushing the NON-ENVELOPED virus through the cell membrane (the whole virus (rare) or just the genome)

virus makes a self-sealing pore on the host membrane
translocation
ENVELOPED VIRUS fuses with the host cell membrane and is relased into the cell
Fusion
ENV or NON-ENV virus sends cascading signal to the host after a speific interaction between the spike proteins and the cell's viral receptor...these signals tell the cell to endocytose thevirus

Unusual process b/c most cells only do pinocytosis
Viropexis
step that relases the viral genome from the capsid
uncoating
uncoating occurs during
viropexis - endocytotic vesicle is ACIDIFIED which disrupts the viral env and cpasid and allows the genome to enter the cytoplasm

fusion - uncoating happens during penetration

translocation - ?
there is no physical evidence of viral infection at what stage of replication
Eclipse
DS DNA genomes of viruses are replicated how?
by semi-conservative replication similiar to cellular DNA synthesis
ss RNA viral genome replication strategies
Positive strand genomic RNA --> needs replicative intermediate (IR)

Negative strand genomic RNA --> must carry RNA polymerase and also needs IR
which RNA genomes have messenger function and can be immediately translated
ss RNA positive
which RAN genomes are anti-sense and have NO messenger function
ss RNA negative
which RNA genome is transcribed within the paritially opened capsid by a polymerase within the capsid (a + RNA strand)
ds segmented reovirus genome
+ RNA strands have 2 functions
1. messenger function --> translated
2. assembles within a prescurser particle in which it serves as a template for the complimentary strand to yeild ds genomic segments
in which viruses can protein synthesis be sequential (synthetic proteins are transcribed befroe the structural proteins)

mRNA is not transcribed all at the same time
DNA virueses
which viruses does the transcription and processing of all proteins occur at eh same time because translating the entire strand as a polyprotein
RNA Viruses
where does synthesis of retroviral RNA occur
in the cytoplasm of the infected cell
RDDP comes from
the infecting virus
RDDP does what
reverse transcribes the +strand RNA into a single strand of complimentary DNA --> forming a heteroduplex within the genomic RNA.....the DNA is then used as a template to make a complimentary DNA resulting in ds DNA.....ds DNA is transported to the nucleus where it is incorporated into the host genome (PROVIRAL DNA).....proviral DNA is reanscribed to RNA to form progeny
how do non-enveloped progeny virions assemble
the structural proteins first self-assemble (NO ENERGY) and then capsomeres self-assemble into capsids....the genome (DNA or RNA) then can penetrate into the hollow capsid
ways for the non-enveloped progeny virions to be relased
Lysis (MOST COMMON)
Reverse endocytosis



in both host cell is killed
how does enveloped progeny virions get realsed
the assembly and realse occur at the same time (slow and continous event)
there is no physical evidence of viral infection at what stage of replication
Eclipse
DS DNA genomes of viruses are replicated how?
by semi-conservative replication similiar to cellular DNA synthesis
ss RNA viral genome replication strategies
Positive strand genomic RNA --> needs replicative intermediate (IR)

Negative strand genomic RNA --> must carry RNA polymerase and also needs IR
which RNA genomes have messenger function and can be immediately translated
ss RNA positive
which RAN genomes are anti-sense and have NO messenger function
ss RNA negative
which RNA genome is transcribed within the paritially opened capsid by a polymerase within the capsid (a + RNA strand)
ds segmented reovirus genome
+ RNA strands have 2 functions
1. messenger function --> translated
2. assembles within a prescurser particle in which it serves as a template for the complimentary strand to yeild ds genomic segments
in which viruses can protein synthesis be sequential (synthetic proteins are transcribed befroe the structural proteins)

mRNA is not transcribed all at the same time
DNA virueses
which viruses does the transcription and processing of all proteins occur at eh same time because translating the entire strand as a polyprotein
RNA Viruses
where does synthesis of retroviral RNA occur
in the cytoplasm of the infected cell
RDDP comes from
the infecting virus
RDDP does what
reverse transcribes the +strand RNA into a single strand of complimentary DNA --> forming a heteroduplex within the genomic RNA.....the DNA is then used as a template to make a complimentary DNA resulting in ds DNA.....ds DNA is transported to the nucleus where it is incorporated into the host genome (PROVIRAL DNA).....proviral DNA is reanscribed to RNA to form progeny
how do non-enveloped progeny virions assemble
the structural proteins first self-assemble (NO ENERGY) and then capsomeres self-assemble into capsids....the genome (DNA or RNA) then can penetrate into the hollow capsid
ways for the non-enveloped progeny virions to be relased
Lysis (MOST COMMON)
Reverse endocytosis



in both host cell is killed
how does enveloped progeny virions get realsed
the assembly and realse occur at the same time (slow and continous event)
what are the 4 different ways that a cell can respond to viral infection
1. no apparent effect --> very low level of viral rep in a secondary target cell (at portal of entry cells)

2. cytopathic effect with eventual cell death --> usual response to primary taregt infection (VERY SPECIFIC)

3. loss of growth control and transformation into a cancer cell --> both RNA and DNA tumor viruses

4. Latent infection --> viral genome remains in cell but an absence of total viral gene expression
viruses are dependent on what to make their protein
HOST
the capacity of a cell to become infected

Means that the cell has receptors to which a particular virus can attach
susceptibility
what type of cell can not be infected because it expresses no receptors for a particular virus
resistant cell
what type of viral infection occurs when the susceptible cell is PERMISSIVE

the cell will make and express all the virally coded proteins
Productive viral infection
what type of viral infection occurs when the complete viral genome is available and the interaction will result in infeabus progeny viruses begin produced and realeased

PRODUCTIVE infection from virus's persceptive
Productive viral infection
what type of viral infection occurs when the cell may be susecptible and allow viral entry or the cell may be NOn-permissive and allow only a few viral genes to be expressed
Abortive Viral infections
what type of viral infection occurs when the infection could be in a permissive or non-permissive cell and the infecting virus lacks a full complement of genes (DEFECTIVE VIRUS), NO progeny produced
Abortive Viral Infection
what type of viral infection occurs when the cells may be only transiently permissive and the consequences are the virus persists in the cell until the cell becomes permissive and only a few cells in a population produce viral progeny at any time
Restrictive/restringent viral infection
what type of viral infection has a very low level of productive infection over an extended period of time
Restrictive/restringent viral infection
what type of viral infection is the latently infected cell nonpermissive and the cell retains the entire viral genome, the cell is also able to express and make some viral proteins and genomes and the cell is not killed
Latent viral infection
what type of viral infection does the latently infected cell allow abortive infection b/c not allowing virulent progeny to be formedbut the genome of the virus can often enter a permissive cell
latent viral infection
what type of viral infection occurs when the infected cell becomes transformed to the malignant state. this cell may or may not be permissive for th eproduction of progeny (RNA tumor viruses are replicated and DNA tumor viruses transform nonpermissive cells)
Oncogeniv transforming viral infection
what type of viral infection occurs when the RNA tumor virus experiences productive infection but the DNA tumor virus experiences abortive infection
oncogenic transforming viral infectrion
what type of viral infection occurs when the cells are never infected by the virus ...most resistance is due to lack of cell surface recptors for a particular virus
cells resistant to viral infection
what type of viral infection occurs when there is no infection, no replication, no progeny virus and a dead end for the virus
cell resistant to viral infection
what are cellular pathways that the viruses can use to mature their mRNA from the nucleus to the cytoplasm
RNA splicing and transport to the cytoplasm
what cleaves host cell nascent transcripts in the cytoplasm
virus encoded endonuclease
does viral or cellular mRNA have a higher affinity for ribosomes
***viral mRNA****

some viruses can change the specificity of the host cell translational appartus in favor of the virus
what is the ususal portal of entry for a virus
external coverings of the body

have a low level of viral replication here (restrictive infection)
how and where does the virus migrate to after entering
goes to lymph nodes where there is a low level of replication and then the virus migrates via the thoracic duct to the circulation (VIREMIC PHASE), the virus then goes in search of target tissue
what type of virus is most likely to induce a B cell response because will eventually o to the spleen
virus in the blood (VIREMIC PHASE)
where does the greatest cytopathic result occur....when have clinical diesease
in the target tissue
the reflection of the time required for the virus to reach its target tissue

measured formt he time of intial infection until signs and symptoms of clinical disease develop
incubation period
if the portal of entry is also the target tissue then the incubation period is
short (2-4 days)
no viremic phase
ie influenza
if the virus must go thru a viremic phase to reach its target tissue then the incubation period is
LONG (14-21 days)
is chicken pox
derived from bone marrow

appear as lymphocytes with numerous cytoplasmic granules

neither T nor B cells-->b/c lacks all of the surface markers associated with either T or B cells (no Igs, CD4/CD8, no T cell receptor complex)

make up 5-20% of the mononuclear cells in the blood and spleen and are rarely found in other lymphoid tissues or organs
NK cells
what do NK cells secrete to give rise to Apoptosis
perforins and granzymes
how do NK cells discriminate between self and nonself
presence or absence of Class I MHC

NK cells target cells that lack self, class I MHC
what are the primary effector functions of NK cells
1. production of pro-inflammatory cytokines--INF gamma and TNF alpha

2. cyttotoxicity of NK cells mediated thru the production of cytotoxic granules that contain perforin and granzymes similer to T cytotoxic cells
what is produced by CD4 cells and NK cells to activate macrophages
INF gamma
what activates NK cells to express INF gamma and also tells the NK cells to proliferate
IL 12 and IL 15
when does induction of NK cell effector functions generally occur
within a day or two after primary viral infection-----long before the adaptive immune response develops
what do NK cells do in the early stages of infection
restrain viral replication before an effective immune response develops
if the number of NK cells decreases then the susceptibility to infection
increases


esp with the herpes viruses: HSV-1, EBV, HCMV
for anti-viral activity are Type 1 or Type 2 INF's more potent
Type 1 INFs are 10 to 100 more potent
what are the 2 Type 1 INFs
1. INF alpha -- produced by mononuclear phagocytes; family of polypeptides

2. INF beta -- produced by many cells best represented by fibroblasts; a single protein

both types share the same cell surface receptor
what are the Type II INFs
INF gamma -- signature cytokine of Th CD4 effector cells
which INFs are not consitutively made....their syntethsis must be induced
Type I Infs
what is the potent inducer of type I INFs
ds RNA
when Type I INFs bind to the cell-surface rector of infected and noninfected cells the transcription of what is promoted
anit-viral protein
what are the 3 anti-viral proteins
1. 2'-5' Oligoadenylate synthetase

2. PKR Kinase

3. Mx Protein
which anti-viral protein polymerizes ATP into a series of 2'-5' linked oligomers---this activates an endonuclease which degrades viral RNA
2'-5' olgioadenylate synthetase
which anti-viral protein phophorylates the eukaryotic protein synthesis initiation factor dF-2 and therefore inhibits the translation of viral proteins
PKR kinase
which anti-viral protein produces cellular resistance specifically to influenza virus replication
Mx Protein
which 2 anti-vrial proteins are activated by engaging ds RNA
2-5 oligoadenylate synthetase
PKR kinase
the more class I MHC molecules that are expressed on a virally infected cell, the ?????? likely it is that an anitgen-sensitive T cell will recognize the virally infected cell and respond to it
MORE ****
which INFs induce the increased expression of class I MHC molecules on virally infected cells and surrounding cells that may become infected
Type I INFs
what are 2 excellent immunogens that can induce a B cell mediated Ig response
viral peplomers and capsid proteins

ONLY IF EXTRACELLULAR
what type of Igs can prevent viral infection of susceptible cells
neutralizing Igs
what type of Igs are specific for structural viral proteins and can facilitate phagocytosis of virus particles
non-neutralizing Igs
how can T cells recognize virally infected cells
peptide fragments from viral proteins are displayed by class I and II MHC molecules on the surface of the infected cell
what type of effector T cell consititutes the primary defense against virally infected cells
CD8 effector T Cells because almost all nucleated cells express Class I MHC
how can CD8 T cells elminate virus-infected cells
1. release of perforins

2. induction of apoptosis by at least 2 different mechanisms
what type of immune response is essential for the elimination of virally infected cells and recovery from viral disease
cell-mediated response because once the cell is infected Igs are of little defense
what are 4 properties that are present in cells but not in viruses
no ribosomes
no mitochondria
no/few enzymes
no binary fission or mitosis
what type of viruses HAVE to replicate in the nucleus
DNA viruses (except pox viruses)
name the family of viruses:

used to be papovaviridae family

nonenvel, icosahedral

ds DNA, supercoiled circle

rep in nucleus (early and late transcription)

long incubation

proliferative
papillomavaviridae
proliferative squamous lesions (cutaneous or mucosal)

usually BENIGN some undergo malignant transformation
Paillomas (warts)
cutaneous papillomas are described as being
plantar, common, flat
mucosal papillomas are described as being in the
oral cavity, larynx, and anogenital area
how are papillomas transmitted
person-person and indirect
HPV are classified into different types based on ?
DNA sequence homology and serology

Oral HPV = HPV6,11
Cervical dysplasia = HPV16, 18, 6, 11
HPV may play a major role in development of a variety of ?????, esp ?????
carcinomas, cervical neoplasia
at least 85% of cervical carcinomas contain ??? DNA rather than circular, extrachromosomal DNA
intergrated HPV DNA
what 2 HPV 16 and HPV 18 proteins are oncogenes? What can they bind to and inactivate and what does this do to the cell?
E6 and E7 (expressed from early genes)

Binds to and inactivates the cellular growth suppressor proteins p53 and p105RB. the cell then becomes more susceptible to mutation, chromosomal aberrations, or action of a cofactor leading to cancer


p53 and p105RB are normal cell proteins that allow for routine cell replication ---> cellular growth cycle policemen
****WARTS FREQUENTLY UNDERGO???****
SPONTANOEOUS REGRESSION
what are some ways to treat warts
topical (salicyclic acid, formalin)
surgical
cryotherapy (freezing off)
laser therapy
interferon injections
what does the current HPV vaccine consist of? When should it be given?
non-infectious virus like particles (VLPs)

3-dose series given to girls 11-12 or as a catch up ages 13-26


***DOES NOT TREAT EXSISTING HPV INFECTIONS, GENITAL WARTS, PRECANCERS, CANCERS****
what family of viruses was originally isolated in respiratory secretions and adenoid tissues

capable of eliciting tumore in animal hosts only

being currently studied as potential vectors for gene replacement therapy (cystic fibrosis)

nonenveloped, icosahedral

linear ds DNA

rep in nucleus (early and late transc)

ubiquitous

can establish a latent infection in tonsils and adenoids
adenoviridae
how is adenoviridae transmitted
direct....respiratory droplets and fecal matter
what are the main clinical manifestations of adenovirus
1. endemic respiratory disease
2. phayngoconjunctival fever
3. acute follicular conjunctivitis
4. epidemic keratoconjunctivitis
5. acute respiratory disease
6. gastroenteritis
7. acute hemorrhagic cystitis
8. systemic infection in immunocomp pts
9. obesity?
what is the most common adenoviral eye infection and how is it transmitted? unilateral or bilateral?
acute follicular conjuncitivitis

direct contact

unilateral
ship-yard worker's disease

unilateral or bilateral

adenovirus

ocular trauma causes, then direct inoculation will predispose to disease
epidemic keratoconjuncitivitis
what type of adenovirus manifestation is common in military recruits
acute respiratory diesease
what types of vaccine is available for adenovirus
oral vaccine

lyophylized live viruses in enteric capsule

d/c in 1999
what family of viruses is the simplest animal DNA virus

non-envel, icosahedral

ss DNA linear with 2 coat proteins

rep in nucleus
Parvoviridae
what are the 2 members of the parvoviridae family
parvovirus genus
dependovirus genus
which parvoviridae virus replicates autonomously in rapidly dividing cells
parvovirus (human parvo virus B19)
which parvoviridae virus replicates only in the prescence of a helper viruse (usually adenovirus)
dependovirus
how is human parvovirus B19transmitted?
respiratory, blood transfusions, vertically from mother to fetus
what cells does Human parvovirus B19 target? and why?
*****immature cells in the erythroid lineage (pre-RBCs)*****

b/c rapidly dividing
what are the clinical mainfestations of human parvovirus B19
1. erythema infectiosum (fifth disease)
2. transient aplastic crisis
3. infection in immunodeficient pts
4. infection during pregnancy
what is the most common human parvo b19 manifestation

in early school age children (rare in adults)

mild constitutional symptoms PLUS RASH**

joint involvement in adults
erythema infectiosum (fifth disease)
which human parvo b19 manifestation lowers the production of RBCs and may produce crisis in chronic hemolytic anemia pts (SICKLE CELL PTS)
transient aplastic crisis
immunocompromised pts with human parvo b19 can develop
chronic supression of bone marrow and chronic anemia
infection of human parvo b19 during pregnancy can lead to
hydrops fetalis and fetal death
what family of viruses have a **** double envelope not derived from any host cell membrane (entirely de novo synthesis)****

ds linear DNA

rep in cytoplasm ** in areas called "virus factories"

***does not need any of the cell's nuclear enzymes for transc, rep of DNA***...still need ribosome from host
Poxviridae
what are the 3 stages of poxviridae Transcription
1. immediate early
2. early
3. late
contagious, febrile disease characterized by vesicular and pustular lesions
smallpox (variola)
smallpox is considered by the CDC to be a
Catergory A biological agent
how is smallpox transmitted
directly (resp.)

humans are the only natural host
what is the smallpox vaccine
live vaccinia virus

causes a limited infection that creates a cross-reaction with smallpox
which type of virus family has 3 subfamilies

ubiquitous

enveloped, icosahedral

rep in nucleus

envelope from nuclear (not cytoplasmic) membrane

ds linear DNA

CAN CAUSE LATENT INFECTIONS ****
Herpesviridae
3 subfamilies of herpesviridae
alpha
beta
gamma
alpha Herpes viruses
HSV 1 and 2
Varicella zoster virus (ZVZ, HSV 3)
what is the primary target of alphs herpes viruese
mucoepithelial cells
what is the site of latency for alpha herpes viruses
neuron
how is HSV 1 and 2 transmitted
direct contact , sex
how is HSV3 and ZVZ transmitted
close contact, respiratory
what is the primary infection of HSV 1 and 2
herpetic gingivostomatitis, labialis, and gentialia
what is the primary infection of VZV and HSV3
chicken pox and if reactivated shingles
what are the beta herpesviruses
Cytomegalovirus (CMV, HHV5)
Human herpesvirus 6 (HHV6)
Human herpesvirus 7 (HHV7)
what is the primary target cell of cytomegalovirus
monocyte, lymphocyte, epithelial cells
what is the primart target cell of HHV 6 and 7
T cells and ???
what is the site of latency of CMV
monocyte, lymphocyte and ???
what is the site of latency for HHV6 and HHV7
t cells and???
how is CMV transmitted
close contact, transfusions, tissue transplant, congenital
how is HHV6 and HHV 7 transmitted
respitatory and close contact?
What is the main clinical manifestations of CMV
cytomegalic inclusion disease, mononucleosis
what is the main clinical manifestations of HHV6
exanthem subitum (roseola, sixth disease)
what are the gamma herpes viruses
Epstein Barr virus (EBV)
Human Herpervirus 8 (Kaposi's sarcoma-associated viruse, KSVH, HHV8)
what is the primary target cell of EBV
B cells and epithlial cells
What is the primary target cell of HHV8
lymphocytes
what is the site of latentcy of EBV
B Cell
What is main clinical manifestations of EBV
infectious mononucleosis, Burkitt's lymphoma, oral hairy leukoplakia, poat-transplantation lymphoproliferative disorder
What is the main clinical manifestations of HHV8
AIDS assoicated Kaposi's syndromwe
how is EBV transmitted
saliva
how is HHV8 transmitted
close contact (sex), saliva?
what holds the space between the capsid and the envelope
tegument proteins
how does herpesvirus get into the cell
FUSION
how does herpesvirus get realsed from the cell
BUDDING
how are HSV viral genes transcribed
cell RNA polymerase II
primar infection with this usually occurs in childhood via contact with infected adults....primary infection is asymp but some are life threatening
HSV-1
usually acquired later in life, slightly more common in women
HSV2
infection occuring in absence of detectable abs against HSV, symptomatic cases last 2-3 weeks
primary infection
generally milder than symp primary infections,

may be either reactivation of latent HSV from primary infection or reinfection by a different strain of HSV

1 week duration
recurrent infection
in what order do the Igs respond to HSV
IgM-->IgG-->neutralizing abs (B and D)
What are the primary clinical manifestations of HSV1
orofacial lesions
-acute primary herpetic gingivostomatitis
- recurrent herpes labialis
what are the primary clinical manifestations of HSV2
genital lesions but can occur as orofacial lesions
what is the most common herpetic infection of early childhood

soreness of mouth, fever, malaise, irritability

cervical lymph node enlargement

eruption of multiple vesicular lesions

localized or throughout the oral cavity
acute primary herpetic gingivpstomatitis
what occurs with every case of acute primary herpetic gingivostomatitis
gingivitis (may bleed spontaneously)
"fever blisters"

"cold Sores"

usually mild, NO fever

few lesions in isolated areas

often a PRODROME - itching, burning at site

No systemic signs usually
Recurrent herpes labialis
what are all the clincial manifestations of HSV
1. orofacial infections
2. ocular infections (keratoconjunctivitis)
3. gential infections
4. traumatic infections
5. encephalitis
6. neonatal herpes
7. eczema herpeticum
8. disseminated, systemic disease in immunocom pts
how does the HSV manifestationof keratoconjunctivitis usually come about
usually result of auotinoculation during gingivostomatitis....BUT can be acquired at birth from mother with genital infection
corneal involvement-->dendritic ulcer fomration followed by keratitis

recurrent episodes lead to dense scarring, loss of sight
Kerotoconjunctivitis
What do you NEVER treat Kerotoconjunctivitis with
corticosteriods
pathology and pathogenesis of ????? is essentially the same as HSV orofacial infections
gential infections (herpes genitalis)
early symptoms: itching, burning in anogenital area, pain in legs, butt, genital area, vaginal fluid discharge, abdominal pressure

development of vesicular lesions

fever, headache, swollen lymph nodes in groin area
primary infection of herpes genitalis
milder infection

sometimes no visible lesions

virus shedding from cervix may be asymp

potential problem at term in pregnant women
recurrent infection of herpes genitalis
introduction of HSv into microabrasion or wounds on hands, fingers
herpetic whitlow
what type of viruses are HSV1 and HSV2

----they remain latent in regional sensory ganglia
neurotropic
how do you distinguish between HSV 1 and HSV2 in the lab
genotyping
how is VZV transmitted
via contact with infected secretions or air droplets (dried scabs are NOT infective--unlike smallpox)
how does VZV enter and how does it spread
thru URT, oropharynx then disseminates through lymph and blood (viremia) then spreads centrifugally beginning on trunk and neck, the vesicles may occur in the mouth, nose, of throat