This document discusses antiviral drugs and their mechanisms of action. It describes several classes of antiviral drugs that target different stages of the viral lifecycle, including nucleoside analog reverse transcriptase inhibitors (NRTIs), protease inhibitors, and DNA polymerase inhibitors. Specific drugs mentioned include acyclovir, ganciclovir, didanosine, zidovudine, lamivudine, saquinavir, indinavir, and ritonavir. It provides details on how these drugs work, such as by incorporating into viral DNA/inhibiting viral enzymes or being phosphorylated into active metabolites that inhibit viral replication. The document also discusses treatment of various viral infections including HIV, hepatitis
Antiviral Drugs – A Brief (Classification & Mechanism of Actions)Parth Thosani
This presentation gives you an overview of antiviral agents (both retro and non-retro viruses), focusing on the sites of actions, classification and class-wise mechanism of actions.
This PPT covers Drug therapy for Viral Infection or disease. It includes Viral replication cycle, classification of antiviral drugs, Anti-Herpes drug, Anti Influenza drugs, Anti hepatitis drugs and anti retroviral drugs
Antiviral Drugs – A Brief (Classification & Mechanism of Actions)Parth Thosani
This presentation gives you an overview of antiviral agents (both retro and non-retro viruses), focusing on the sites of actions, classification and class-wise mechanism of actions.
This PPT covers Drug therapy for Viral Infection or disease. It includes Viral replication cycle, classification of antiviral drugs, Anti-Herpes drug, Anti Influenza drugs, Anti hepatitis drugs and anti retroviral drugs
Antiviral drugs are a class of medications used to treat viral infections by inhibiting the replication or growth of viruses in the body. These drugs work by targeting specific components of a virus, such as the viral enzymes, proteins, or nucleic acids, and disrupting their ability to infect or replicate inside host cells. This can help reduce the severity of symptoms, prevent complications, and speed up recovery.
There are many types of antiviral drugs available, including:
1. Nucleoside or nucleotide analogues: These drugs mimic the structure of the nucleosides or nucleotides needed for viral replication, thereby interfering with virus replication.
2. Protease inhibitors: These drugs block the activity of viral proteases, which are enzymes that are required for the replication and assembly of some viruses.
3. Interferons: These drugs are naturally occurring proteins that help the immune system fight viral infections by boosting the body's antiviral response.
4. Neuraminidase inhibitors: These drugs block the activity of viral neuraminidase, an enzyme that is required for the release of virus particles from infected cells.
5. Fusion inhibitors: These drugs block the fusion of viral and host cell membranes, which is an essential step in viral entry and replication.
Antiviral drugs can be used to treat a variety of viral infections, including influenza, HIV/AIDS, hepatitis B and C, herpes, and Ebola. However, the effectiveness of these drugs can vary depending on the specific virus and the stage of infection. Antiviral drugs may also have side effects, and it is important to consult with a healthcare provider before taking them.
I have tried to provide an outline regarding the general antivirals available in our country..and discussed regarding MOA,indications and Therapeutic uses.
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mainly includes structures, SAR , mechanism of action, uses and toxicity of antiviral drugs
Antiviral drugs are a class of medication used specifically for treating viral infections rather than bacterial ones. Most antivirals are used for specific viral infections, while a broad-spectrum antiviral is effective against a wide range of viruses.
classification of antiviral agents,replication of HIV virus and replication of virus.targets of virus,classification of antiviral agents with structure and mechanism action of antiviral agents
Introduction to virus & antivirals.
Treatment of Influenza virus.
Treatment of RSV
Viruses are intracellular parasites with no metabolic machinery of their own.
Lack cell wall & cell membrane.
To replicate, viruses must attach to & enter a living host cell – animal, plant, or bacterium – and use its metabolic process.
Viral replication requires DNA or RNA synthesis.
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This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
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June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
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Biological screening of herbal drugs: Introduction and Need for
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Natural Products, In vitro evaluation techniques for Antioxidants, Antimicrobial and Anticancer drugs. In vivo evaluation techniques
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This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
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Antiviral Agents
ANTIVIRAL DRUGS AND GENERAL MECHANISM
These are the agents used in the treatment of viral infections.
Viruses are obligate intracellular parasites that depend on metabolic processes of host cells for their
replication. Virus consist of either RNA or DNA enclosed in a protein coat and a lipoprotein coat.
PATHOGENIC VIRUSES:
DNA viruses:
o Poxviruses: smallpox,
o Herpesviruses (Vercella Zoster, H. Simplex, CMV): chickenpox, shingles, cold sores,
glandular fever),
o adenoviruses (sore throat, conjunctivitis) and
o papillomaviruses (warts).
RNA viruses:
o orthomyxoviruses (influenza),
o paramyxoviruses (measles, mumps, respiratory tract infections),
o rubella virus (German measles),
o rhabdoviruses (rabies),
o picornaviruses (colds, meningitis, poliomyelitis),
o retroviruses (acquired immunodeficiency syndrome [AIDS], T-cell leukaemia),
o arenaviruses (meningitis, Lassa fever),
o hepadnaviruses (serum hepatitis) and
o arboviruses (arthropod-borne encephalitis and various febrile illnesses, e.g. yellow
fever).
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LIFE CYCLE OF VIRUSES AND THEIR HOST CELLS:
1. ATTACHMENT
Formed vacuoles. Attachment is facilitated by poly peptide binding site on the envelop or
capside wich interact with the receptor of host cell.
These receptors are generally for cytokines, NTs, hormone, and ion channels.
Reduce the attachment ----immune gamma-glycoproteins
Agents inhibiting host cell penetration by virus. e.g. HBIG (Hepatitis B immunoglobulin),
HRIG (Human rabies immunoglobulin), Varicella-Zoster immunoglobulin.
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Example of viral infection and Receptor
a. HIV: Helper T-lymphocytes CD4 glycoprotein,
CCR5 receptor for chemokines MCP-1 and RANTES,
CXCR4 chemokine receptor for cytokine SDF-1.
b. Rebies virus: Acetylcholine receptor on skeletal muscle.
c. Adenovirus: MHC molecules.
d. Infantile diarrhoea virus: β-Adrenoceptors.
2. UNCOATING – Uncoating of viral DNA/RNA by host cell
The formed virus-receptor complex enter to the host cell by receptor mediated endocytosis after
removal of coat by host enzyme.
Prevented by Amentadine/Rimentadine (used in RTI, influenza, Resp. Syncital virus)
Agents binding to surface coats of viruses and stabilising the protein coat so that subsequent
uncoating of virus in host cell does not occur. e.g. Disoxaril.
3. REPLICATION, SYNTHESIS AND PROTEIN SYNTHESIS:
a. Reverse Transcriptase
Viral RNA produces vDNA by Reverse transcriptase enzyme that is inhibited by Reverese
transcriptase (vRNA dependent DNA polymerase) inhibitor (Anti-retro virus—RNA virus):
o NRTIs -Nucleoside RTIs: Zidovudine (AZT), Lamivudine, Stavudine, Didanosin,
Abacavir
o Non NRTIs: Nevirapine, Delavirdine, efavirenz
b. Protease Inhibitor (HIV 1- protease inhibitor)- “NAVIR”
A protease (also called a peptidase or proteinase) is any enzyme that performs
proteolysis; protein catabolism by hydrolysis of peptide bonds
Protease inhibitors prevent viral replication by selectively binding to viral
proteases (e.g. HIV-1 protease) and blocking proteolytic cleavage of protein precursors
that are necessary for the production of infectious viral particles. EX- Ritonavir,
indinavir, Saquinavir, Lopinavir
Hepatitis C virus NS3/4A protease inhibitor- “PREVIR”): asunaprevir, boceprevir,
grazoprevir, paritaprevir, simeprevir
c. DNA Synthesis Inhibitors
Inhibit the DNA synthesis (Anti-Herpes simplex and cytomegalovirus CMVvirus):
Idoxuridine, Vidarabine, Acyclovir, Ganciclovir.
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HSV1- oral, ocular, and Facial infection
HSV2- Genital infection
d. vRNA polymerase inhibitor (Anti-Herpes virus)- Foscarnate
e. Protein Synthasis inhibitor
Agent inducing production of intracellular enzymes which inhibit the translation of viral-
mRNA to viral protein. e.g. Human leucocyte interferon.
Agent inhibiting 'late' structural protein synthesis in Variola virus. e.g. Methisazone
4. ASSEMBLY- by virus particle and budding
Agents preventing assembly of enveloped mature viral particles. e.g. Rifampicin
Amentadine: inhibit the maturation of viral protein
5. RELEASE- by lysis
CLASSIFICATION:
A) ACCORDING TO MECHANISM OF ACTION:
1. Nucleoside reverse transcriptase inhibitors
A) Purine nucleoside and nucelotides: Acyclovir, Ganciclovir, Famiciclovir.
B) Pyrimidine nucleoside and nucelotides: Idoxuridine, Trifluouridine
C) Thiosemicarbazones: Methisazone
D) Miscellaneous: Foscarnet sodium, ribavirin
B) ACCORDING TO ENZYME INHIBITION :
1. DNA polymerase inhibition: Idoxuridine, Trifluouridine
2. Reverse transcriptase inhibitors : Zidovudine, Stavudine.
C) According to the treatment protocol antiviral agents
I. Treatment of respiratory virus infection
Adamantane derivatives: Amantadine, Rimantadine
II. Treatment of herpes and cytomegalo viruse infection.
a. Purine nucleotides: Acyclovir, Ganciclovir, Vidarabine.
b. Pyrimidine nucleosides: Trifluouridine, Idoxuridine.
c. Phosphorus derivatives: Foscarnet sodium.
III. Treatment of HIV infections
a. RT inhibition.
1. Purine derivatives: Didanosine.
2. Pyrimidine derivative: Zidovudine, Stavudine.
3. Non-nucleosides: Nevirapine, Delaviridine, Efavirenz.
b. Protease inhibition: Saquinavir, Indinavir, Ritonavir, Nelfinavir, Amprenavir, Lopinavir.
c. Integration inhibition: Zintevir.
IV. Treatment of Hepatitis C virus infections
a. PREVIR: asunaprevir, boceprevir, grazoprevir, paritaprevir, simeprevir
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ANTIVIRAL DRUGS
I. Adamantane
Active only against influenza - A virus. It is also used in the management ofParkinson’s
disease (Stimulates the release of dopamine nerve terminal and inhibit the presynaptic
reuptake.
MOA
Amantadine and Rimantadine inhibit the initiation of transcription (vRNA to vDNA)
of an early stage between uncoating and viral specific RNA synthesis.
They inhibit the viral replication by interfering with the influenza A virus M2 prortein
(integral membrane protein) further leads to interfere with the uncoating process and
prevent the viral particle assembling during replication.
Uses: influenza, RTI, Resp. Syncital virus infection. Also used in idiopathic parkinsonism.
A) Amantadine hydrochloride
B) Rimantadine hydrochloride
C) Idoxuridine trifluoride
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MOA:
It is a substituted pyrimidine (Thymidine) analogue and Inhibit DNA synthesis by
inhibiting the thymidylate phosphorylase and vDNA polymerase.
Idoxuridine gets phosphorylated within the cell and the triphosphate derivative is
incorporated into DNA (of both viral and mammalian). Such DNA is more susceptible
to breakage and results in faulty transcription.
Uses : Used in the treatment of superficial H. simplex keratoconjunctivitis as 0.5% eye
ointment applied every 4 hrs during day and once at bedtime or as 0.1% eyedrops, 1 drop
instilled in conjunctival sac every hour during day and every 2 hours during night.
D) Aciclovir
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Synthesis:
MOA:
It is active against Herpes viruses particularly Herpes simplex virus (HSV) type-l and
type-2.
The Herpes viruses contain a specific thymidine kinase which phosphorylates acyclovir
to its monophosphate. Further phosphorylation is by host cell guanosine
monophosphate kinase to the diphosphate, which is then phosphorylated to acyclovir
triphosphate. Acyclovir triphosphate inhibit Herpes virus DNA polymerase. It also get
incorporated into viral DNA and terminates biosynthesis of viral DNA strand.
Acyclovir----thymidine kinase (viral)-A. monophosphate-----Guanosine monophosphate
kinase--- A.diP----- Acyclovir triphosphate---inhibit virus DNA polymerase
Uses: It is used in the treatment of infections due to Herpes simplex virus and Varicella-
Zoster virus and Epstein virus.
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E)Gancyclovir
MOA: It is a synthetic guanine derivative. It converts into its active metabolite Ganciclovir-5-
triphosphate which inhibits the vDNA polymerase.
Uses: Used to treatment of cytomegalovirus (CMV) infection in immune compromised
patients.
F) Didanosine
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MOA: It is an inosine analogue. Mechanism of action is similar to zidovudine (Inhibits the
Reverse Transcriptase Enzyme which responsible for conversion of vRNA to vDNA
Didanosine-------T. kinase---- Dideoxyadenosine triphosphate ----inhibit RT
Uses : It is used in the treatment of AIDS. It is also used as an antiviral agent, antimetabolite,
antineoplastic agents.
G) Zalcitabine
MOA: it converted into active metabolite dideoxycytidine 5’-triphosphate and interfere with
the reverse transcriptase enzyme by competing for natural substrate deoxycytidine 5’-
triphosphate and further inhibit the DNA Synthesis.
Uses: Along with Zidovudine (AZT), for treatment of HIV infection. And also, useful as
antiretroviral protease inhibitor.
H) Lamivudine
MOA: It is a synthetic nucleotide analogue and phosphorylated intracellularly to its active 5’-
triphosphate derivative and inhibit the HIV reverse transcriptase enzyme and HBV polymerase,
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resulting in DNA chain termination.
Uses: Used in treatment of HIV infection and Hepatitis-B infection
I) Loviride
MOA: Inhibit the reverse transcriptase enzyme and inhibit the DNA replication
Uses: in HIV infection and chronic Hepatitis-B infection
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J) Delavirdin
N-[2-[4-[3-(propan-2-ylamino)pyridin-2-yl]piperazine-1-carbonyl]-1H-
indol-5-yl]methanesulfonamide
MOA: Inhibit the reverse transcriptase enzyme and inhibit the DNA replication
Uses: used in HIV infection along with other antiviral drugs.
K) Ribavirin
1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxy methyl) oxolan-2-yl]-1,2,4-
triazole-3-carboxamide
MOA: inhibits the viral mRNA polymerase
Uses: Treatment of Influenza A and B and used in sever RTI.
II. Retroviral Protease Inhibitors
MOA: They inhibit the viral protease enzyme which responsible for proteolysis of large of
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polyprotein molecules to functional viral protein particles.
Uses: Mostly used in HIV-1 infection with immunodeficiency along with antiretroviral
nucleoside analogues.
L) Saquinavir
N-[4-[(3-(tert-butylcarbamoyl)-3,4,4a,5,6,7,8,8a-octahydro-1H-isoquinolin-2-yl]-3-
hydroxy- 1-phenylbutan-2-yl]-2-(quinoline-2-carbonylamino) butanediamide
M) Indinavir
1-[4-benzyl-2-hydroxy-5-[[(2-hydroxy-2,3-dihydro-1H-inden-1-
yl]amino]-5-oxopentyl]-N-tert-butyl-4-(pyridin-3-yl
methyl)piperazine-2-carboxamide
N) Ritonavir
1,3-thiazol-5-ylmethyl N-[3-hydroxy-5-(3-methyl-2-[[methyl-[(2-propan-2-
yl-1,3-thiazol-4-yl)methyl]carbamoyl]amino]butanoyl]amino]-1,6-
diphenylhexan-2-yl] carbamate.