Viral Skin and Soft Tissue Infections Flashcards

1
Q

What are the three subfamilies of Herpesviruses? How many are considered human herpesviruses?

A
  1. Alphaherpesviruses
  2. Betaherpesviruses
  3. Gammaherpesviruses

8 are considered human herpes viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What three viruses fall in the alpha herpesvirus family?

A

Herpes Simplex Virus 1 (HSV-1)
Herpes Simplex Virus 2 (HSV-2)
Varicella-Zoster Virus (VZV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the B virus?

A

A monkey alpha herpesvirus which can infect humans only by bite, and can result in fatal encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What three viruses fall in the beta herpesvirus family?

A

Cytomegalovirus (CMV)
Human Herpesvirus 6A and 6B (HHV-6A, HHV-6B)
Human Herpesvirus 7 (HHV-7)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What two viruses fall in the gamma herpesvirus family?

A

Epstein-Barr Virus (EBV)

Human Herpesvirus 8 (HHV-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes herpes labialis, and what age group does it affect most?

A

HSV-1 more often than HSV-2, “cold sores”

Affects children and adolescents most

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes genital herpes?

A

HSV-2 > HSV-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is another common HSV-1 complication?

A

Keratoconjunctivitis, which can cause blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some of the rarer HSV-1 complications?

A

dermatitis, encephalitis, disseminated HSV (in immunocompromised)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Who is most likely to be infected with a systemic HSV-2 infection which is very dangerous?

A

Neonates, general herpes and encephalitis can be very severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the definition of HSV latency?

A

Continued presence of viral genome in lysogenic cycle, in the absence of viral replication / particles. Latency always happens and lasts a lifetime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does HSV latency initially occur?

A

HSV enters into nerve cells, is transported to the relevant sensory ganglion, and viral replication occurs in the ganglion for several days before latency occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When does HSV reactivation occur? What initiates it and where does it occur?

A

Spontaneously, often induced by sunburn, stress, menstruation, or immunocompromisation

Activated by a neuron-specific JNK kinase pathway

Virus replicates and travels back down the axon to cause infection by the site of primary infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the structure of HSV and its genome?

A

Large, enveloped DNA virus with icosahedral capsid

Linear, ds DNA genome with about 80 genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the process of HSV attachment to integration into genome?

A

Virion attaches via heparan sulfate on cell surface, and is either endocytosed or directly fuses with virion envelope.

Capsid is transported to nuclear pore via microtubules, and released into the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three phases of HSV gene expression?

A
  1. Immediate early genes adapt cell for virus replication
  2. Early genes produce / replicate viral DNA
  3. Late genes include structural proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is the viral DNA packaged into capsids and then ultimately released?

A

In the nucleus, packaged into capsids.

Naked capsid passes into cytoplasm via temporary envelop of nuclear membrane, then is finally enveloped via Golgi apparatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are two key HSV-coded enzymes?

A
  1. DNA Polymerase

2. Thymidine Kinase (TK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the mechanism of acyclovir?

A

Nucleotide analog to thymidine.

Phosphorylated by HSV’s TK to acyclovir monophosphate, then made into triphosphate by cellular kinases.

This acyclovir-trisphosphate functions to:

  1. inhibit viral DNA polymerase
  2. terminate nascent viral DNA strands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is valacyclovir? Does this work on latent virus?

A

The prodrug form of acyclovir with higher bioavailability

Neither this or acyclovir will work on latent virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are complications of varicella?

A

Pneumonia, inflammation of brain or spinal cord, congenital birth defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does latent VZV stay?

A

Dorsal root ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Varicella, and how is it transmitted? (include first infection to a second infection)

A

Chickenpox
Virus which initially enters upper respiratory tract, spreads to lymphoid organs and replicates there

Second stage spreads to epithelial tissue causing lesions and respiratory tract for further transmissino

24
Q

What is the incubation period of varicella, and how do the lesions progression?

A

12-14 days, lesions progress centrifugally (trunk first, then outward to face and limbs).

Macule -> papule -> vesicle -> crusting which heals without scarring

25
What is Zoster and how does it typically begin?
Shingles, recurrence of latent VZV | Typically begins with nerve pain / post-herpetic neuralgia
26
Where does Zoster occur? How can it be prevented?
Lesions are generally limited to skin / mucous membrane innervated by reactivated ganglion It can happen multiple times, and is preventable via Zostervax, a stronger version of childhood chickenpox vaccine
27
What are the general characteristics of beta herpesvirus infections?
Restricted host range and cell type specificity
28
What is HHV-6A vs HHV-6B vs HHV-7? What is the relative prevalence?
HHV-6: wide cell tropism, preferential T cell replication. HHV-6A - no clear disease association HHV-6B - associated with exanthem subitum (roseola), stays latent in monocytes / macrophages HHV-7 - T cell tropic, latent in T cells Most people are seropositive for both
29
What is the clinical presentation of Exanthem subitum (roseola)?
Common childhood infection | Fever lasts 3-5 days, followed by a rash as fever diminishes, accompanied by upper respiratory symptoms
30
What are complications of roseola?
High fever, aseptic meningitis, hepatitis, mononucleosis-like syndrome
31
Where is HHV-8 of high prevalence? What class of herpesviruses is it?
Gamma herpesviruses HIgh prevalence in sub-Saharan Africa and Mediterranean region, low prevalence elsewhere except HIV-1 positive
32
What is HHV-8 associated with?
Kaposi's sarcoma, and lymphomas / lymphoid hyperplasia
33
What is Classic Kaposi's Sarcoma (KS)?
Slow progression, typically found in Mediterranean men, nodular / plaque-like dermal lesion in lower leg
34
What is Endemic-African KS?
More aggressive KS, with lymph node involvement
35
What is Iatrogenic KS?
Induced via solid-organ transplant patients (immunocompromised), common in Mediterranean
36
What is the lymphadenopathic form of KS and who is it typically foundin?
Disseminated and aggressive, involving internal organs, viscera, lymph nodes, and skin Seen in HIV patients
37
What is the structure of papillomaviruses?
Non-enveloped icosahedral | Circular dsDNA with 8-10 genes
38
What are papillomaviruses known for?
Cutaneous and mucosal warts, condylomas (genital wards), and papillomas
39
What are the two major transforming genes of the HPV-16 genome?
E6: Causes destruction of p53 tumor suppressor protein E7: Inactivates Rb tumor suppressor protein (controls G1->S)
40
What is the major vaccine target of HPV?
L1 gene product, a major capsid protein, active component of Gardasil HPV vaccine
41
What types of cutaneous warts does HPV cause? What is one HPV type common to cause this?
Common wart - painless and hyperkeratotic Plantar wart - painful, deeply set on weight-bearing surfaces of foot Flat warts - multiple flat, assymmetric papules HPV 2 commonly causes this
42
What types of mucosal warts does HPV cause? What HPV types are associated with these and cancer?
Laryngeal, oral, and conjuctival papillomas -> HPV 6 and 11 Anogenital papillomas -> 6 and 11 also cause these, but weak cancer association Types 16 and 18 are uncommon but papillomas often progress to cervical cancer
43
What is the range of clinical outcomes to HPV infection?
Subclinical infection with full clearance to high grade lesions with carcinoma
44
What are condylomata?
plural of condyloma, or genital warts (includes anus)
45
Where does HPV infection occur in the skin? What does it initially do? How is it spread?
The basal cell layer (quite superficial) Initially induces hyperplastic growth to keep the skin growing fast for viral spread Mature virus is only released in highly keratinotic cells (stratum corneum), and is spread by direct contact or fomites
46
What stage of HPV Cervical Intraepithelial Neoplasia (CIN) is difficult to differentiate from condylomata? What does this correspond to?
CIN1, about 1/3 of the stratum layer is abnormal thick and hyperplasic
47
What are the next stages of CIN?
CIN2 = 2/3 of skin CIN3 = 3/3 of skin = carcinoma in situ Invasive cancer -> infects lower tissue Metastatic cancer -> invades other body tissues
48
What is Gardasil protective against? Cervarix? How young can they be?
Gardasil - HPV types 6,11,16, and 18 Cervarix - HPV 16 and 18 (just cancer) Can be as young as 9 years old
49
What is the structure of Picornaviruses and what is one example?
Small, non-enveloped viruses with ssRNA (+) genomes example: Coxsackieviruses (especially A)
50
How are picornaviruses spread?
Saliva, mucous, or feces
51
What are two diseases caused by picornaviruses?
1. Hand, Foot, and Mouth Disease - blisters / ulcers on all these areas, typical in Asia 2. Herpangina - includes only the mouth lesions
52
What are general clinical symptoms of Coxsackie virus infections?
Common in infants in children, general malaise like fever, sore throat, headache, vomiting, convulsions Specifically: Small papulovesicular lesions on tonsils and soft palate, as well as hands and feet in HFMD. Lesions heal within 1-5 days. Rapid resolution vs HSV infection
53
What is vaccinia virus used for?
Live virus used to immunize against smallpox (Variola). Temporary skin lesion is left.
54
What is molluscum contagiosum?
A type of Poxvirus, leaves Wart-like bumps which resolve in 6-12 weeks, spread by contact
55
What is orf?
A zoonotic poxvirus which can be spread via sheep / goats.