HSV-2 Activators
Herpes Simplex Virus Type 2 (HSV-2) is a highly prevalent viral pathogen primarily associated with genital herpes infections, although it can also cause infections in other body areas. HSV-2 is characterized by its ability to establish latency, a state in which the virus remains dormant within host neuronal cells, evading the immune system's full response. During latency, limited viral gene expression occurs, which is crucial for maintaining the virus within the host. This strategy allows HSV-2 to persist for the host's lifetime, with periodic reactivations that lead to symptomatic outbreaks or asymptomatic viral shedding. The virus's life cycle includes attachment to host cells, entry, replication, assembly, and release of new viral particles. HSV-2 has evolved sophisticated mechanisms to manipulate host cellular machinery for its replication and spread, making it a subject of extensive research to understand viral pathogenesis and host-virus interactions.
The activation of HSV-2 from latency, leading to productive viral replication and subsequent disease manifestation, is influenced by various cellular and molecular triggers. Stress, immunosuppression, hormonal changes, and other physiological or environmental factors can initiate the reactivation process. Activation involves the upregulation of the immediate-early viral genes, which encode regulatory proteins essential for initiating the viral replication cycle. These proteins act as transactivators for other viral genes, including early and late genes responsible for DNA replication, capsid assembly, and viral particle formation. The reactivation from latency is a complex process that requires the precise regulation of viral and host factors. For example, changes in cellular signaling pathways, such as those mediated by protein kinase C (PKC) and the mitogen-activated protein kinase (MAPK) pathways, have been implicated in the reactivation of HSV-2. These pathways can be influenced by cellular stress responses, providing a link between the host's physiological state and viral reactivation. Understanding the mechanisms underlying HSV-2 activation from latency is critical for developing strategies to manage HSV-2-related diseases, focusing on the intricate balance between viral latency and reactivation.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol is a polyphenolic compound known for its role in activating SIRT1, a class III histone deacetylase. This activation enhances autophagy through the AMPK-mTOR pathway, indirectly promoting HSV-2 activation by facilitating viral replication through improved cellular resource availability. | ||||||
Trichostatin A | 58880-19-6 | sc-3511 sc-3511A sc-3511B sc-3511C sc-3511D | 1 mg 5 mg 10 mg 25 mg 50 mg | $149.00 $470.00 $620.00 $1199.00 $2090.00 | 33 | |
Trichostatin A, an HDAC inhibitor, modulates chromatin structure by inhibiting histone deacetylation. This epigenetic alteration can indirectly activate HSV-2 by facilitating viral gene expression through enhanced accessibility of the viral genome. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
SB203580, a p38 MAPK inhibitor, disrupts the p38 MAPK signaling pathway. This disruption can indirectly activate HSV-2 by preventing the inhibition of viral gene expression, as p38 MAPK is implicated in the regulation of viral transcriptional repression. | ||||||
Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
Wortmannin inhibits phosphoinositide 3-kinase (PI3K), a key regulator of the Akt pathway. Inhibition of PI3K can indirectly activate HSV-2 by impeding the anti-viral effects mediated by Akt, thereby promoting viral replication through reduced cellular defense mechanisms. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $36.00 $68.00 $107.00 $214.00 $234.00 $862.00 $1968.00 | 47 | |
Curcumin modulates NF-κB signaling by inhibiting IκB kinase. This modulation can indirectly activate HSV-2 by enhancing the transcription of viral genes, as NF-κB plays a pivotal role in regulating the expression of various genes involved in the immune response and viral replication. | ||||||
5-Azacytidine | 320-67-2 | sc-221003 | 500 mg | $280.00 | 4 | |
5-Azacytidine, a DNA methyltransferase inhibitor, induces DNA demethylation. This epigenetic modification can indirectly activate HSV-2 by promoting the expression of viral genes through increased accessibility of the viral genome. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002 inhibits PI3K, disrupting the PI3K-Akt signaling pathway. This disruption can indirectly activate HSV-2 by suppressing the anti-viral effects mediated by Akt, leading to enhanced viral replication through compromised cellular defense mechanisms. | ||||||
BAY 11-7082 | 19542-67-7 | sc-200615B sc-200615 sc-200615A | 5 mg 10 mg 50 mg | $61.00 $83.00 $349.00 | 155 | |
BAY 11-7082 inhibits NF-κB activation by targeting IκBα phosphorylation. This inhibition can indirectly activate HSV-2 by preventing the suppression of viral gene expression, as NF-κB is involved in regulating the transcription of genes related to the immune response and viral replication. | ||||||
SP600125 | 129-56-6 | sc-200635 sc-200635A | 10 mg 50 mg | $40.00 $150.00 | 257 | |
SP600125 is a JNK inhibitor that disrupts the JNK signaling pathway. This disruption can indirectly activate HSV-2 by impeding the anti-viral effects mediated by JNK, facilitating viral replication through reduced cellular defense mechanisms. | ||||||
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
ATRA influences cellular differentiation by binding to retinoic acid receptors (RARs). This influence can indirectly activate HSV-2 by altering the cellular environment, making it more conducive for viral replication through the modulation of host cell differentiation and function. | ||||||