Abstract
The skin is the largest organ in the human body, acts as our fist line of defense, and has a sophisticated array of cells and signaling molecules to help protect the body from infection. Yet even with this sophisticated defense, viruses cause a range of cutaneous diseases in humans, many of which are widespread in the population and cause significant morbidity and mortality, along with psychological and financial repercussions. Each virus has unique mechanisms by which it evades the immune system, replicates, and spreads. Some viruses infect the skin directly while others gain access systemically first. Infections can be acute or subclinical and then resolve, while others are persistent or can remain latent for years. This spectrum of presentations is mirrored by an equally wide array of evasion tactics that the viruses use to manipulate and escape both the adaptive and innate immune responses. In addition to highlighting viral responses, particular attention is also paid to the local immune response generated in the skin. Five viruses will be discussed in detail: herpes simplex virus, varicella zoster virus, human immunodeficiency virus, molluscum contagiosum virus, and human papilloma virus; along with the latest information on the development and advancement of both therapeutic and prophylactic vaccines.
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Questions
Questions
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1.
Herpes simplex virus produces latency associated transcripts (LATs) which have been found in high concentrations in latently infected neurons. LATs help to increase the efficiency of latency and subsequent reactivation by what mechanism?
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A.
By interfering with production and secretion of IL-1 and TNF-α
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B.
By destroying the homing receptor (CLA) on CD8+ T cells
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C.
By inhibiting the production of proteins involved in the apoptosis pathway
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D.
By altering the activity of neutrophils, macrophages, and NK cells
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A.
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Answer/Explanation: answer C
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The herpes simplex virus does alter the activity of neutrophils, macrophages, and NK cells. As such, it does interfere with the production and secretion of some pro-inflammatory cytokines, such as IL-1 and TNF. However, LATs are directly responsible for inhibiting granzyme-B and capsase-8 mediated apoptosis
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2.
Depletion of what cell line has been implicated with the enhanced survival, prolonged course of infection, and oncogenic transformation associated with some high risk HPV types?
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A.
T helper cell
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B.
Langerhans cell
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C.
Macrophage
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D.
NK cell
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A.
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Answer/Explanation: answer B
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Depletion of Langerhans cells has been documented in HPV infections along with a lack of expression of certain cell signaling molecules (CD54, CD86, TNF-α, etc.). Cumulatively, these features decrease the antigen-presenting capacity of Langerhans cells and can induce immune tolerance and ultimately oncogenic transformation
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3.
The early peak in viral replication that is integral for large scale HIV amplification and chronic viral persistence is directly attributable to infection of what cell line?
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A.
CD4+CCR5+ T cells in the intestinal mucosa
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B.
Dendritic cells (DC) located in draining lymph nodes
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C.
CD4+ ICAM1+ T cells in keratinocytes
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D.
Effector Th cells in mucosal surfaces
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A.
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Answer/Explanation: answer A
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HIV does initially infect DC and exploits their natural trafficking properties to transfer virus to CD4+ T cells in draining lymph nodes. However, the cell line directly responsible for the early peak in viral replication is infection of CD4+CCR5+ T cells in the lamina propria of intestinal mucosa. The collection of T cells here exceeds the total number of T cells in all other body sites combined and is responsible for the early and massive amplification of the virus
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Kollipara, R. et al. (2017). Immunodermatology and Viral Skin Infection. In: Gaspari, A., Tyring, S., Kaplan, D. (eds) Clinical and Basic Immunodermatology. Springer, Cham. https://doi.org/10.1007/978-3-319-29785-9_17
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