Introduction:
Herpes Labialis, also known as the cold sore, is characterized by painful clusters of clear blisters on or around the mouth, and is often accompanied with fever. The disease is usually caused by the virus HSV-1, or herpes simplex type 1, but can also be caused by HSV-2. In a previous study, it was found that 67.6% of Americans possessed antibodies for HSV-1, establishing HSV-1 as an exceptionally prevalent virus even in developed countries 9. The virus is spread through skin to skin contact between an individual exhibiting viral shedding, and an unaffected person, but can also be contracted through exposure to surfaces that contain the virus. Once HSV-1 is contracted, there is no way to eliminate the virus from the body. However, …show more content…
It consists of an icosadeltahedral capsid that houses the dsDNA, a proteinaceous tegument, which surrounds the capsid and contains proteins that aid viral replication, and an envelope with glycoproteins. To gain entry into the human host cell, viral glycoprotein C binds heparan sulfate or chondroitin sulfate on human cellular glycoproteins. Next, viral glycoprotein D, which is associated with glycoprotein H and L, binds a coreceptor, and the viral envelope fuses with the cell membrane, releasing the capsid and tegument into the host. Tegmental protein VHS disassembles cytosolic ribosomes and digests RNA, thwarting host protein production. Cellular microtubules ferry the capsid to nuclear pores where tegmental proteins facilitate the transfer of viral DNA into the cell nucleus. In the nucleus, the viral dsDNA becomes circular, and is bound by transcription factors OCT1, α-TIF, and C1, which facilitate transcription of α genes by RNA Polymerase II. α genes produce regulatory proteins that serve as inhibitors of their own production and activate transcription of β and γ genes. β genes correspond to proteins involved with nucleotide synthesis and DNA replication. These facilitate replication of the viral genome. β proteins facilitate transcription of γ genes. These genes are associated with proteins in the capsid. The capsid is constructed around the viral DNA, and are bound by tegmental proteins in the nucleus. The …show more content…
The first change includes nuclear swelling and clumping of chromatin to produce a fiberglass appearance in the nucleus, which is accompanied with hydropic changes in the cytoplasm. Affected cells often exhibit reticular ballooning and reticular degeneration. Ballooning degeneration is characterized by cell swelling and detachment from neighboring cells, increasing eosinophilicity, multinucleation, and cytoplasmic homogenization. Reticular degeneration involves cell swelling due to vacuolization (this causes the cytoplasm to appear clear), and cell lysis. Eosinophilic inclusion bodies form in the nucleus, which are composed of aggregated viral proteins. Epithelial cell lysis among cells that are in close proximity leads to the development of fused, multinucleated supercells. Transparent vesicular fluid, the virus-rich contents of the cells, accumulates between the dermal and epidermal layers, and is what leads to the blistered appearance of a cold sore. Neutrophils and lymphocytes are also present in vesicular fluid as they aggregate around lysed cells to remove cell contents
Herpes Labialis, also known as the cold sore, is characterized by painful clusters of clear blisters on or around the mouth, and is often accompanied with fever. The disease is usually caused by the virus HSV-1, or herpes simplex type 1, but can also be caused by HSV-2. In a previous study, it was found that 67.6% of Americans possessed antibodies for HSV-1, establishing HSV-1 as an exceptionally prevalent virus even in developed countries 9. The virus is spread through skin to skin contact between an individual exhibiting viral shedding, and an unaffected person, but can also be contracted through exposure to surfaces that contain the virus. Once HSV-1 is contracted, there is no way to eliminate the virus from the body. However, …show more content…
It consists of an icosadeltahedral capsid that houses the dsDNA, a proteinaceous tegument, which surrounds the capsid and contains proteins that aid viral replication, and an envelope with glycoproteins. To gain entry into the human host cell, viral glycoprotein C binds heparan sulfate or chondroitin sulfate on human cellular glycoproteins. Next, viral glycoprotein D, which is associated with glycoprotein H and L, binds a coreceptor, and the viral envelope fuses with the cell membrane, releasing the capsid and tegument into the host. Tegmental protein VHS disassembles cytosolic ribosomes and digests RNA, thwarting host protein production. Cellular microtubules ferry the capsid to nuclear pores where tegmental proteins facilitate the transfer of viral DNA into the cell nucleus. In the nucleus, the viral dsDNA becomes circular, and is bound by transcription factors OCT1, α-TIF, and C1, which facilitate transcription of α genes by RNA Polymerase II. α genes produce regulatory proteins that serve as inhibitors of their own production and activate transcription of β and γ genes. β genes correspond to proteins involved with nucleotide synthesis and DNA replication. These facilitate replication of the viral genome. β proteins facilitate transcription of γ genes. These genes are associated with proteins in the capsid. The capsid is constructed around the viral DNA, and are bound by tegmental proteins in the nucleus. The …show more content…
The first change includes nuclear swelling and clumping of chromatin to produce a fiberglass appearance in the nucleus, which is accompanied with hydropic changes in the cytoplasm. Affected cells often exhibit reticular ballooning and reticular degeneration. Ballooning degeneration is characterized by cell swelling and detachment from neighboring cells, increasing eosinophilicity, multinucleation, and cytoplasmic homogenization. Reticular degeneration involves cell swelling due to vacuolization (this causes the cytoplasm to appear clear), and cell lysis. Eosinophilic inclusion bodies form in the nucleus, which are composed of aggregated viral proteins. Epithelial cell lysis among cells that are in close proximity leads to the development of fused, multinucleated supercells. Transparent vesicular fluid, the virus-rich contents of the cells, accumulates between the dermal and epidermal layers, and is what leads to the blistered appearance of a cold sore. Neutrophils and lymphocytes are also present in vesicular fluid as they aggregate around lysed cells to remove cell contents