Herpesvirus important properties
1. Structure
a. Large 120 – 200 nm
2. Capsid and genome
a. Icosahedral nucleocapsid
b. Linear double-stranded DNA
c. No polymerase
3. Viral envelope
a. Enveloped
b. Acquire lipoprotein envelope by budding through host cell
nuclear membranes, instead of outer membrane
4. Tegument
a. Tegument is present between nucleocapsid and envelope
b. It contains essential regulatory proteins, transcription
translation factors
c. Vital role in replication
Replication and cellular effects
1. Intranuclear replication
a. Replicate within nucleus
b. Form intranuclear inclusions
2. Cellular changes
a. 4 main types infection produce multinucleated giant cells
b. 4 types are
i. HSV 1 and 2
ii. Varicella zoster
iii. Cytomegalovirus
3. Superantigens
a. Cytomegalovirus and Epstein-barr produce superantigens
Latency and subclassification
Its hallmark is to cause latent infections
After acute disease, virus enters latent state. Then asymptomatic period
Virus may reactivate later on
Subdivided into 3 categories based on type of cells infected
1. Alpha herpesvirus
a. HSV 1 2 and varicella zoster
b. Epithelial cells infected
c. Latency in sensory neurons
, 2. Beta herpesviruss
a. Cytomegalovirus and HHV-6
b. Variety of tissues infected and established latency in them
3. Gamma herpesvirus
a. Epstein-Barr and HHV-8
b. Infect and establish latency in lymphoid cells
Pathogens and oncogenesis
6 important pathogens in this family; HSV 1,2, varicella zoster,
cytomegalovirus (CMV), EBV, HHV-8.
Medically significant property oncogenic
EBV burkitt’s lymphoma, naspharyngeal carcinoma
HHV-8 Kaposi sarcoma
Transmission and pathogenesis
1. Herpes simplex viruses
a. Transmission
i. HSV 1 saliva
ii. HSV2 sexual contact
iii. Oral-genital contact causes HSV1 on genitals, HSV2
on oral cavity
iv. Asymptomatic shedding transmits both types
v. HSV2 transmit to neonates via
1. Vesicular lesions
2. Asymptomatic shedding
b. Pathogenesis
i. Replicates in skin/mucous membranes
ii. Causes vesicular lesions containing serous fluid filled
with virus particles
iii. Virus then migrates up through retrograde axonal flow
iv. Latency established in sensory neurons
v. HSV1 trigeminal ganglia
vi. HSV2 lumbar and sacral ganglia
vii. Noncoding RNAs called LATS suppress viral replication
in latency
viii. Triggers may reactivate virus, like trauma
2. Varicella zoster virus
a. Transmission
i. Respiratory droplets
ii. Direct contact through lesions
1. Structure
a. Large 120 – 200 nm
2. Capsid and genome
a. Icosahedral nucleocapsid
b. Linear double-stranded DNA
c. No polymerase
3. Viral envelope
a. Enveloped
b. Acquire lipoprotein envelope by budding through host cell
nuclear membranes, instead of outer membrane
4. Tegument
a. Tegument is present between nucleocapsid and envelope
b. It contains essential regulatory proteins, transcription
translation factors
c. Vital role in replication
Replication and cellular effects
1. Intranuclear replication
a. Replicate within nucleus
b. Form intranuclear inclusions
2. Cellular changes
a. 4 main types infection produce multinucleated giant cells
b. 4 types are
i. HSV 1 and 2
ii. Varicella zoster
iii. Cytomegalovirus
3. Superantigens
a. Cytomegalovirus and Epstein-barr produce superantigens
Latency and subclassification
Its hallmark is to cause latent infections
After acute disease, virus enters latent state. Then asymptomatic period
Virus may reactivate later on
Subdivided into 3 categories based on type of cells infected
1. Alpha herpesvirus
a. HSV 1 2 and varicella zoster
b. Epithelial cells infected
c. Latency in sensory neurons
, 2. Beta herpesviruss
a. Cytomegalovirus and HHV-6
b. Variety of tissues infected and established latency in them
3. Gamma herpesvirus
a. Epstein-Barr and HHV-8
b. Infect and establish latency in lymphoid cells
Pathogens and oncogenesis
6 important pathogens in this family; HSV 1,2, varicella zoster,
cytomegalovirus (CMV), EBV, HHV-8.
Medically significant property oncogenic
EBV burkitt’s lymphoma, naspharyngeal carcinoma
HHV-8 Kaposi sarcoma
Transmission and pathogenesis
1. Herpes simplex viruses
a. Transmission
i. HSV 1 saliva
ii. HSV2 sexual contact
iii. Oral-genital contact causes HSV1 on genitals, HSV2
on oral cavity
iv. Asymptomatic shedding transmits both types
v. HSV2 transmit to neonates via
1. Vesicular lesions
2. Asymptomatic shedding
b. Pathogenesis
i. Replicates in skin/mucous membranes
ii. Causes vesicular lesions containing serous fluid filled
with virus particles
iii. Virus then migrates up through retrograde axonal flow
iv. Latency established in sensory neurons
v. HSV1 trigeminal ganglia
vi. HSV2 lumbar and sacral ganglia
vii. Noncoding RNAs called LATS suppress viral replication
in latency
viii. Triggers may reactivate virus, like trauma
2. Varicella zoster virus
a. Transmission
i. Respiratory droplets
ii. Direct contact through lesions
