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Antivirals | HIV, Hepatitis, Influenza, Herpes Treatment

Ninja Nerd・105 minutes read

Antivirals are vital in combating various viruses like HIV, influenza, hepatitis, and herpes through mechanisms like inhibiting specific enzymes essential for viral replication. Understanding the mechanisms of action and adverse effects of these drugs is crucial for effective treatment against viral infections.

Insights

  • Antivirals play a crucial role in combating viruses like HIV, influenza, hepatitis, and herpes by targeting specific viral mechanisms and enzymes.
  • Understanding the mechanisms of action of antiviral drugs, such as entry inhibitors, reverse transcriptase inhibitors, and protease inhibitors, is essential for effectively combating viral infections.
  • Adverse effects of antiviral drugs, including mitochondrial toxicity, pancreatitis, nephrotoxicity, bone marrow suppression, and hypersensitivity reactions, highlight the importance of monitoring and managing potential side effects.
  • Different viruses like HIV, hepatitis B, hepatitis C, and herpes have distinct life cycles and target specific tissues, necessitating tailored antiviral treatments to inhibit viral replication and spread effectively.
  • Treatment strategies for viral infections involve a combination of antiviral drugs targeting various viral enzymes, such as reverse transcriptase, protease, and DNA polymerase, to prevent viral replication and limit infection, with considerations for genotype-specific therapies and potential adverse effects.

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Recent questions

  • What are the key mechanisms of antiviral drugs?

    Antivirals combat viruses like HIV, influenza, hepatitis, and herpes by targeting specific viral components. HIV, for example, uses proteins like gp41 and gp120 to bind with receptors on immune cells, while entry inhibitors like enfuvirtide block viral RNA entry. Drugs like maraviroc inhibit virus docking, and reverse transcriptase inhibitors like zidovudine impede DNA formation. Understanding these mechanisms is crucial in effectively combating viral infections.

  • How do integrase inhibitors work in preventing viral replication?

    Integrase inhibitors like dolutegravir hinder the integration of viral DNA into host cell DNA, preventing viral replication. By targeting the enzyme responsible for this process, these inhibitors effectively stop the virus from incorporating its genetic material into the host cell's DNA, thereby halting continuous viral replication.

  • What is the significance of ribavirin in treating hepatitis C?

    Ribavirin is used in refractory HCV cases alongside other medications to inhibit RNA replication. By targeting inosine monophosphate dehydrogenase, ribavirin prevents the virus from replicating its genetic material. While effective in treating HCV, ribavirin can be teratogenic and cause hemolytic anemia as adverse effects.

  • How do protease inhibitors function in combating viral infections?

    Protease inhibitors like ritonavir work by inhibiting the enzyme responsible for cleaving viral polyproteins into functional proteins. By blocking this crucial step in viral replication, these inhibitors prevent the virus from producing essential proteins needed for its survival. However, they can lead to adverse effects like CYP450 inhibition and lipodystrophy.

  • What are the adverse effects associated with nucleoside reverse transcriptase inhibitors?

    NRTIs like zidovudine and abacavir can cause mitochondrial toxicity, while stavudine and didanosine may induce pancreatitis. Tenofovir is linked to nephrotoxicity and acute kidney injury, and zidovudine can lead to bone marrow suppression. Abacavir, on the other hand, can trigger a severe hypersensitivity reaction due to the HLA-B 5701 gene. Monitoring for these adverse effects is crucial during antiviral therapy.

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Summary

00:00

"Antivirals: Crucial Tools Against Viral Infections"

  • Antivirals are crucial in combating various viruses like HIV, influenza, hepatitis, and herpes.
  • HIV, a retrovirus, targets T helper cells in the immune system, utilizing proteins like gp41 and gp120 to bind with CD4 and CCR5/CXCR4 receptors.
  • Entry inhibitors like enfuvirtide prevent viral RNA from entering host cells by blocking fusion with CD4.
  • Maraviroc hinders virus docking by inhibiting gp120 from binding with CCR5 receptors.
  • Reverse transcriptase enzymes convert viral RNA into DNA, which can integrate into host cell DNA, leading to viral replication.
  • Nucleoside reverse transcriptase inhibitors (NRTIs) like zidovudine impede DNA formation by mimicking nucleotides, halting the process.
  • Non-nucleoside reverse transcriptase inhibitors (NNRTIs) like nevirapine bind to an allosteric site on the enzyme, disrupting its function.
  • Integrase enzymes integrate viral DNA into host cell DNA, a process inhibited by integrase inhibitors to prevent viral replication.
  • Inhibiting integrase prevents the incorporation of viral DNA into host DNA, averting continuous viral replication.
  • Understanding the mechanisms of antiviral drugs is vital in combating viral infections effectively.

14:23

HIV Treatment: Inhibitors and Side Effects

  • Integrase inhibitors include dolutegravir, routagravir, and elvatecravir, identified by the common root word "tegravir" in their names.
  • The process of viral DNA transcription involves creating viral RNA, which is then translated into proteins using ribosomes.
  • Proteases are essential enzymes that cleave polyproteins into structural and functional proteins necessary for viral replication.
  • Protease inhibitors like addazanovir, dorinovir, and denver le penavir end in "naveer" and work by inhibiting proteases to prevent protein cleavage.
  • The HIV life cycle involves incorporating viral RNA into the virus in the Golgi apparatus before exocytosis to infect other cells.
  • Highly active antiretroviral therapy (HAART) regimen requires two nucleoside reverse transcriptase inhibitors (NRTIs) and an integrase or protease inhibitor.
  • Adjunct drugs like maravirock and fuvirtide are used in HIV-resistant strains with specific receptor requirements.
  • NRTIs can cause mitochondrial toxicity leading to myopathy, neuropathy, hepatic steatosis, and lactic acidosis.
  • NRTIs like stavudine and didanese can induce pancreatitis, while tenofovir can cause nephrotoxicity and acute kidney injury.
  • Zidovudine may lead to bone marrow suppression, resulting in anemia and neutropenia, while abacavir can trigger a severe hypersensitivity reaction.

27:38

Adverse effects and replication of antiretroviral drugs

  • Adverse effects of NRTIs: mitochondrial toxicity, pancreatitis, nephrotoxicity with tenofovir, bone marrow suppression with zidovudine, hypersensitivity reaction with abacavir due to HLA-B 5701 gene.
  • Adverse effects of NNRTIs: hepatotoxicity, CNS toxicity causing vivid dreams with efavirenz, teratogenic effects with efavirenz and delavirdine.
  • Adverse effects of integrase inhibitors: rhabdomyolysis leading to increased CK levels and myoglobin in urine.
  • Adverse effects of protease inhibitors: crystal-induced nephropathy, acute tubular necrosis, lipodystrophy causing fat accumulation, hyperglycemia due to inhibition of glucose transporters, inhibition of CYP450 enzymes by ritonavir leading to increased drug concentrations.
  • Influenza virus life cycle: entry through respiratory tract, binding to respiratory cells via hemagglutinin and neuraminidases, uncoating through M2 ion channels, release of viral RNA into host cell nucleus for replication.
  • Influenza virus replication: viral RNA combined with host cell proteins in Golgi apparatus to form new virus, release of new virus through fusion with cell membrane.
  • Importance of five prime cap: necessary for viral RNA to interact with host cell ribosomes for protein synthesis.
  • Role of endonuclease: transfers five prime cap from host cell mRNA to viral RNA for protein synthesis.
  • RNA polymerases: utilized for continuous replication of viral RNA in host cell.
  • Formation of new virus: incorporation of viral RNA with structural and functional proteins in Golgi apparatus to create new virus for release and infection of other cells.

40:43

Antiviral Medications Target Influenza and Hepatitis

  • Hemagglutinin protein is stuck to sialic acid, needing neuraminidase to cleave the connection for virus release.
  • M2 ion proton channels aid in RNA release into the cell cytoplasm, followed by the five prime cap process.
  • Amantadine inhibits M2 ion proton channels, crucial for influenza A treatment.
  • Baloxavir inhibits endonuclease, preventing the transfer of the five prime cap from host mRNA to viral RNA.
  • Neuraminidase inhibitors like oseltamivir and zanamivir hinder the release of the virus from the host cell.
  • Adverse effects of amantadine include ataxia, livido reticularis, and QT interval prolongation.
  • Hepatitis B virus targets hepatocytes, utilizing specific protein channels for entry and replication.
  • Reverse transcriptase inhibitors like NRTIs block the conversion of pre-genomic RNA to DNA, hindering viral replication.
  • NRTIs act as nucleotides in DNA synthesis, lacking a hydroxyl group to prevent further DNA strand formation.
  • Understanding the hepatitis B virus life cycle aids in targeting specific steps with antiviral medications.

54:48

Inhibiting Hepatitis C Virus Replication and Spread

  • Reverse transcriptase inhibitors like lamivudine and entecavir inhibit the enzyme, preventing further DNA formation in viruses.
  • Nucleotide reverse transcriptase inhibitors (NTRTIs) like adefovir and tenofovir also halt DNA formation from RNA templates.
  • Adefovir and tenofovir can lead to Fanconi syndrome, causing the excretion of phosphates, glucose, and amino acids in urine.
  • Interferon alpha increases antiviral peptides, inhibits protein synthesis, and boosts MHC-1 complex expression to activate cytotoxic T cells against virus-infected cells.
  • Interferon alpha can be used against hepatitis B and refractory hepatitis C but may cause pancytopenia and teratogenic effects.
  • Hepatitis C virus, an RNA virus, binds to hepatocytes using various receptors and releases its RNA into the host cell cytoplasm.
  • The viral RNA binds to ribosomes on the rough endoplasmic reticulum, leading to the synthesis of polyproteins like NS3, NS4A, NS5A, and NS5B.
  • The NS3/4A protease cleaves the polyprotein into structural and functional proteins essential for virus replication.
  • NS5A and NS5B are enzymes crucial for replicating viral RNA, with inhibitors of these proteins preventing further virus production.
  • Drugs targeting the NS3/4A protease, NS5A, and NS5B can hinder virus replication and spread, ultimately inhibiting the hepatitis C virus.

01:08:36

"Targeting Enzymes to Prevent Viral Replication"

  • Protease inhibitors directly act by inhibiting the ns3 4a protease, preventing the cleavage of polyprotein into structural and functional proteins.
  • Drugs like semeprovere and pareto prevail are examples of protease inhibitors targeting the ns3 4a site.
  • NS5a inhibitors, like ledipasvir and velpatasvir, inhibit the protein involved in RNA replication and viral assembly.
  • NS5b inhibitors, such as phosphavir and dezabovir, target the ns5b enzyme, which acts as an RNA-dependent RNA polymerase.
  • Ribavirin is used in refractory HCV as part of a triple therapy with sofosbuvir and interferon alpha, inhibiting ionosine monophosphate dehydrogenase to prevent RNA replication.
  • Drug combinations depend on the genotype of the hepatitis C virus, with common combinations like sofosbuvir and ledipasvir for specific genotypes.
  • Ribavirin is teratogenic and can cause hemolytic anemia, while other inhibitors are generally well-tolerated.
  • Herpes viruses like HSV and CMV target specific tissues, causing mucocutaneous lesions, esophagitis, and encephalitis.
  • These viruses enter host cells through endocytosis, release DNA into the nucleus, and utilize viral DNA polymerases to replicate.
  • Understanding the mechanisms of action of these drugs is crucial in targeting specific enzymes to prevent viral replication and infection.

01:22:26

"Viral RNA and DNA replication inhibition"

  • Utilize specific types of RNA polymerases to create viral messenger RNA (mRNA).
  • Ribosomes synthesize proteins using the viral mRNA.
  • Proteins synthesized are crucial for creating new viruses, including structural and functional proteins.
  • Incorporate proteins with nucleic acid in the Golgi apparatus to form a new virus.
  • Release the new virus via exocytosis after fusion with the cell membrane.
  • Utilize viral DNA polymerase to replicate DNA for new viruses.
  • Target the viral DNA polymerase to inhibit DNA replication and virus production.
  • Drugs like Sadafavir and Phoscarnate inhibit viral DNA polymerase.
  • Indications for these drugs include CMV infections resistant to Ganciclovir and HSV infections resistant to Acyclovir.
  • Adverse effects include crystal-induced nephropathy with Sadafavir and electrolyte imbalances leading to seizures with Phoscarnate.

01:35:48

Antiviral Drug Mechanisms and Adverse Effects

  • Drugs inhibit viral replication by blocking nucleotide addition to viral DNA, preventing further DNA synthesis.
  • Practice problems involve identifying drugs blocking CD4 gp41 interaction, CCR5 receptor, and reverse transcriptase enzyme.
  • NRTIs like zidovudine, abacavir, lamivudine, stavudine, tenofovir, and didanosine block reverse transcriptase.
  • Mitochondrial toxicity, pancreatitis, nephrotoxicity, and bone marrow suppression are adverse effects of certain drugs.
  • Non-nucleoside reverse transcriptase inhibitors like nevirapine, efavirenz, and delavirdine bind allosteric sites to inhibit enzyme function.
  • Protease inhibitors like ritonavir cause CYP450 inhibition, hyperglycemia, lipodystrophy, and crystal-induced nephropathy.
  • Integrase inhibitors like dolutegravir, raltegravir, and elvitegravir prevent viral DNA integration into host cell DNA.
  • Adverse effects of antiretroviral drugs include rhabdomyolysis, requiring monitoring of CK and urine myoglobin levels.
  • Influenza treatment involves M2 ion channel inhibitors like amantadine, neuraminidase inhibitors like oseltamivir, and endonuclease inhibitors like baloxavir.
  • Hepatitis B and C treatment includes nucleoside and nucleotide inhibitors, protease inhibitors, NS5A and NS5B inhibitors, and interferon alpha.

01:47:06

Antiviral Drugs and Their Adverse Effects

  • Ribavirin can cause teratogenic effects and hemolytic anemia.
  • Treatment for hepatitis C virus depends on the patient's genotype, with different combinations of protease inhibitors, NS5A inhibitors, and NS5B inhibitors.
  • Drugs like foscarnet and cidofovir inhibit viral DNA polymerases in herpes infections, with specific indications for acyclovir resistance and potential adverse effects like seizures and nephropathy.
  • Guanosine analog drugs like acyclovir and valacyclovir inhibit DNA formation in herpes infections, primarily used for HSV infections with adverse effects including nephrotoxicity and increased risk of TTP, while ganciclovir is used for CMV infections with potential bone marrow suppression.
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