Viruses are the smallest infectious agents consisting of genetic material surrounded by a protein coat. They cannot reproduce on their own and must infect a host cell. There are DNA and RNA viruses that cause various diseases. Antiviral drugs target different stages of the viral life cycle, including entry, replication, assembly and release. Examples discussed include nucleoside/non-nucleoside reverse transcriptase inhibitors for HIV, and amantadine/oseltamivir for influenza which interfere with viral uncoating and neuraminidase activity respectively. Interferons are endogenous proteins with broad-spectrum antiviral effects. Acyclovir targets herpes viruses by incorporating into viral DNA. Effective antiviral treatment requires combinations of drugs to prevent
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 – 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.
Antiviral drugs are a class of medication used specifically for treating viral infections.Like antibiotics for bacteria, specific antivirals are used for specific viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic (also termed antibacterial), antifungal and antiparasitic drugs,or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Antivirals also can be found in essential oils of some herbs, such as eucalyptus oil and its constituents.
Hello friends. In this PPT I am talking about Anti-viral drugs drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
ARVs are included in the drugs with narrow therapeutic index. It's important for every doctors and health care workers to understand mechanism of ARV resistance. Video file is available in the following link: http://www.youtube.com/watch?v=TvNOmwRh0I0&feature=player_detailpage
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.
Antiviral drugs are a class of medication used specifically for treating viral infections.Like antibiotics for bacteria, specific antivirals are used for specific viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic (also termed antibacterial), antifungal and antiparasitic drugs,or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Antivirals also can be found in essential oils of some herbs, such as eucalyptus oil and its constituents.
Hello friends. In this PPT I am talking about Anti-viral drugs drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
ARVs are included in the drugs with narrow therapeutic index. It's important for every doctors and health care workers to understand mechanism of ARV resistance. Video file is available in the following link: http://www.youtube.com/watch?v=TvNOmwRh0I0&feature=player_detailpage
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.
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.
Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit its development.
medicinal chemistry of Antiviral drugsFatenAlsadek
medicinal chemistry of antiviral drugs with its chemical structures and how they chemically work
Done by: Faten Al-Sadek , Pharmacy student at Mohammed Al-Mana college for Health Sciences -MACHS
Protozoal infections and antiprotozoal drugs(therapy).Gagandeep Jaiswal
presentation comprising knowledge about various protozoal infections and therapy options available for the treatment of those infections. various different drugs used in the therapy with their proposed mechanism of action. Hope it will be useful for understanding the pharmacology of antiprotozoals.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
3. Viruses are the smallest infective agents,
consisting essentially of nucleic acid (either
RNA or DNA) enclosed in a protein coat or
capsid.
Viral particles consist of two to three
parts:
•Genetic material, either DNA or RNA.
•Protein coat (Capsid), which surrounds and
protects the genetic material.
•Envelope of lipid , lipid layer that surround
the protein coat when they are outside cell.
Introduction to Virus
4. Viruses do not have metabolic machinery and
cannot reproduce on their own.
It must attach to and enter a host cell. It then
uses the host cell’s energy to synthesize
protein, DNA, and RNA. Viruses are difficult
to kill because they live inside the cells. Any
drug that kills a virus may also kill cells
A fully assembled infectious virus is known
as “virion” which Often contain crucial virus
specific enzymes and visible by electron
microscopy.
Cont.
5. Some Important Examples of Viruses and the
Diseases They Cause are as Follows:
DNA viruses RNA viruses
Pox viruses (smallpox) Orthomyxo viruses (influenza)
Herpes viruses (chickenpox, herpes
etc)
Paramyxo viruses (measles, mumps)
Adenoviruses (sore throat,
conjunctivitis)
Rubella virus (German measles)
Hepa dna viruses (serum hepatitis) Rhabdo viruses (rabies)
Papilloma viruses (warts) Picorna viruses(colds, meningitis,
poliomyelitis)
Retroviruses (AIDS, T-cell leukemia)
Arena viruses (meningitis, Lassa fever)
Arbo viruses (arthropod-borne
encephalitis, yellow fever)
6. Routes of Virus Transfer
• Skin contact
• Respiratory
• Faecal
• Oral
• Milk
• Transplacental
• Sexual
• Insect vector
• Animal bite
9. Antiviral Therapy
• Through vaccination
• Antiviral drug therapy
• Host immune system stimulation
Ideal Antiviral Agents
• Low toxicity to host
• Greater selectivity
• Should kill latent viruses as well
Drawbacks of Antiviral Drug Therapy
• Antiviral drugs are toxic to host cells
• Some viruses multiply in both cytoplasm as well as nucleus
• Antiviral drugs most effective during rapid multiplications
• Latent virus not affected by antiviral drugs
16. Pharmacokinetics of Acyclovir :
• Oral bioavailability ~ 20-30%
• Distribution in all body tissues including CNS
• Renal excretion: > 80 %
• Half life: 2-5 hours
• Administration: Topical, Oral , IV
Uses of Acyclovir:
Primary Genital Herpes
• 5% ointment locally 6 times a day for 10 days
• 1gm/day in 5 divided doses
Recurrent Genital Herpes
• 5mg/kg IV infused over 1 hr
• Repeated 8 hourly for 10 days
17. Mucocutaneous Herpes Keratoconjuctivitis (Localized To Lips And
Lungs)
• 5% ointment locally 6 times a day for 5days
• 1gm/day in 5 divided doses
Chickenpox
• 15mg/kg/day for 7days
Varicella Zoster
• 15mg/kg/day for 7days
• 10mg/kg/8hr IV for 10 days
Herpes Simplex Encephalitis
• Acyclovir 10mg/kg/8hr IV for 10 days
Cont.
18. Adverse Effects
• Stinging and burning sensation
• Nausea, Vomiting, Diarrhea, Headache, Malaise
• Vomiting, Rash, Sweating, Hypotension
• Renal dysfunction, Neurotoxicity
• Myelosuppression – Neutropenia and thrombocytopenia – Ganciclovir
Congeners of Acyclovir
• Valacyclovir is a prodrug of Acyclovir with better bioavailability.
• Famciclovir is hydrolyzed to Penciclovir and has greatest bioavailability.
• Penciclovir is used only topically whereas Famciclovir can be
administered orally.
19. Antiviral Spectrum :
• Acyclovir : HSV-1, HSV-2, VZV, Shingles.
• Ganciclovir / Cidofovir : CMV
• Famciclovir : Herpes genitalis and shingles
• Foscarnet : HSV, VZV, CMV, HIV
• Penciclovir : Herpes labialis
• Trifluridine : Herpetic keratoconjunctivitis
Therapeutic Uses :
Ganciclovir is the drug of choice for:
• CMV retinitis in immunocompromised patient
• Prevention of CMV disease in transplant patients
20. Mechanism of Resistance to Acyclovir
• Impaired production of thymidine kinase.
• Altered thymidine kinase substrate specificity (phosphorylation of
thymidine but not of acyclovir).
• Altered viral DNA polymerase by point mutations and base insertion or
deletions in corresponding genes.
21. Acts against respiratory viral infections Influenza –
• Amantadine / Rimantadine
• Oseltamivir / Zanamavir (Neuraminidase inhibitors)
Acts against RSV bronchiolitis –
• Ribavirin
Amantadine (Amantrel)
Influenza B is not affected as antiviral activity is strain specific.
• Prevention & Treatment of influenza A
• Inhibition of viral uncoating by inhibiting the viral membrane protein
M2(matrix protein) of Influenza A virus . Due to interruption of function of
the M2 protein, the drugs inhibit the acid (H+)-mediated dissociation of the
ribonucleoprotein (RNP) complex early in the process of replication.
• Amantadine also has anti- parkinsonian effect.
Anti-Influenza Virus Drugs
22. Pharmacokinetics of Amantadine
• Oral bioavailability ~ 50-90%
• Amantadine cross extensively BBB whereas Rimantadine does not cross
extensively
• Administration: Oral.
Adverse Effects
• GI intolerance
• CNS side effects
• Anticholinergic effects
• Teratogenic
Uses
Prophylaxis of influenza A2
Treatment of influenza A2
Dose 100mg BD
Contraindications
Epilepsy and other CNS disease, gastric ulcer, pregnancy.
23. Rimantadine (Flumadine)
Methyl derivative of Amantadine.
Interfere with virus uncoating by inhibiting release of specific protein also
its more effective than Amantadine.
More potent, Long acting.
Less side effects and less neurotoxic, High GIT intolerance.
Dose 100mg BD.
Cont.
24. Oseltamivir (Tamiflu)
Sialic acid analogue with braod spectrum activity covering infleunza A,
H5N1(bird flu), H1N1(swine flu) strains and influenza B.
First orally active neuraminidase (NA) inhibitor. A prodrug compound.
Hydrolysis of the ester takes place in the body to give the active carboxylic
acid derivative of Oseltamivir.
As a structural analogue of a key intermediate in sialic acid/NA chemistry,
oseltamivir serves as a competitive inhibitor of viral NA by binding strongly
to the active site of NA. This interaction ultimately prevents the release of
new viral particles from the host cell.
Dose-75 mg oral BD for 5 days.
Cont.
25. Zanamivir (Relenza)
Effective for both influenza A and B.
• Poor bioavailability and poor plasma portion binding
• Use oral inhalation.
No conformational change required to allow binding while oseltamivir
requires change in active sites for binding. Hence, does not tightly bind than
zanamivir leads to differences in development of resistance.
Contraindicated in asthmatics, can induce bronchospasm.
Cont.
26. Adefovir dipivoxil
•Adenosine analogue
•Nucleotide inhibitor
•Mechanism of action: It is phosphorylated to adefovir diphosphate
incorporated into viral DNA termination of further DNA synthesis
prevents viral replication.
•Both decreased viral load and improved liver function.
•Indicated in chronic hepatitis B, also in Lamivudine resistant cases and in
concurrent HIV infection.
Anti-Hepatitis Virus/ Nonselective Antiviral
Drugs
27. Its plasma t½ is 7 hours; intracellular t½ of the diphosphate is upto 18
hours.
Adverse effects:
• Sore throat, headache, weakness, abdominal pain and flu syndrome
• Nephrotoxicity ( higher doses and in those with preexisting renal
insufficiency )
• Lactic acidosis ( patients receiving anti-HIV drugs ).
Dose-10mg/day
Cont.
28. •Cytokines produced by host cells in response to viral infections and other
inducers
•Three types of human IFNs (α, β and γ) are known to have antiviral activity
Mechanism of action:
Induction of host cell enzymes that inhibit viral RNA translation
degradation of viral mRNA and tRNA
Interferon receptors are JAK-STAT tyrosine protein kinase receptors
which on activation phosphorylate cellular proteins .
These then migrate to the nucleus and induce transcription of ‘interferon-
induced- proteins’ which exert antiviral effects.
Interferon α
29. Uses of Interferon α
Chronic hepatitis B-IFNα2A
Chronic hepatitis C-IFNα2B
AIDS-related Kaposi’s sarcoma
Condyloma acuminata
H. simplex, H. zoster and CMV
Pharmacokinetics
Not active orally; administered subcutaneously, or intravenously
High cellular uptake and metabolism by the liver and kidney, less plasma
level
Negligible renal elimination occurs.
30. Adverse Effects of IFN
Flu-like symptoms: fatigue, aches and pains, malaise, fever, dizziness,
anorexia, nausea, taste and visual disturbances develop few hours after each
injection, but become milder later
Neurotoxicity: numbness, neuropathy, altered behaviour, mental
depression, tremor, sleepiness, rarely convulsions
Myelo suppression: dose dependent neutropenia, thrombocytopenia
Thyroid dysfunction (hypo as well as hyper)
Hypotension, transient arrhythmias, alopecia and liver dysfunction.
Drug Interaction:
• It interferes with hepatic drug metabolism
• Toxic accumulations of theophylline
• It may also potentiate the myelosuppression caused by other bone marrow
depressing agents ( Zidovudine )
31. • Aim of anti-HIV therapy is to cause maximal suppression of viral
replication for the maximal period of time that is possible.
• ARV drugs are always used in combination of at least 3 drugs and
regimens have to be changed over time due to development of resistance.
• Life long therapy is required.
The established targets for anti-HIV attack are:
1. HIV Reverse Transcriptase
2. HIV Protease
3. Fusion of viral envelope with plasma membrane of CD4 cells through
which RNA enters the cell.
4. Chemokine Co-Receptor (CCR5) on the host cells which provide
anchorage for surface proteins of virus
5. HIV Integrase
Anti-Retrovirus Drugs
32.
33. Nucleoside Reverse Transcriptase Inhibitors
(NRTIs)
Zidovudine:
•It is a thymidine analogue (azido- thymidine/ AZT), the prototype NRTI.
•After phosphorylation in the host cell - Zidovudine triphosphate selectively
inhibits viral reverse transcriptase in preference to cellular DNA polymerase
Single-stranded viral RNA
Double-stranded proviral DNA
Virus directed reverse transcriptase
(inhibited by Zidovudine triphosphate)
34. Pharmacokinetics:
Rapid oral absorption, but bioavailability is ~65%
It is quickly cleared by hepatic glucuronidation (t1⁄2 1 hr); 15–20% of the
unchanged drug along with the metabolite is excreted in urine
Plasma protein binding is 30% and CSF level is ~50% of that in plasma
It crosses placenta and is found in milk.
Adverse effects:
Anaemia and neutropenia
Nausea, anorexia, abdominal pain, headache, insomnia and myalgia are
common at the start of therapy, but diminish later
Myopathy, pigmentation of nails, lactic acidosis, hepatomegaly,
convulsions and encephalopathy are infrequent.
35. Uses
Zidovudine is used in HIV infected patients only in combination with at
least 2 other ARV drugs
It is one of the two optional NRTIs used by NACO for its first line triple
drug ARV regimen
AZT also reduces neurological manifestations of AIDS and new Kaposi’s
lesions do not appear
AZT, along with two other ARV drugs is the standard choice for post-
exposure prophylaxis of HIV, as well as for mother to offspring
transmission.
36. Interactions:
Paracetamol increases AZT toxicity, probably by competing for
glucuronidation
Azole antifungals also inhibit AZT metabolism
Other nephrotoxic and myelosuppressive drugs and Probenecid enhance
toxicity
Stavudine and Zidovudine exhibit mutual antagonism by competing for
the same activation pathway.
37. Non-nucleoside reverse transcriptase
inhibitors (NNRTIs)
Nevirapine (NVP), Efavirenz (EFV) & Delavirdine
Enzyme inducers, and cause autoinduction of their own metabolism
Nevirapine is started at a lower dose (200 mg/day); the dose is doubled
after 2 weeks when its blood levels go down
Rifampin induces NVP metabolism and makes it ineffective, but has little
effect on EFV levels
Either NVP or EFV is included in the first line triple drug regimen used by
NACO
38. Nevirapine
Rashes are the commonest adverse effect, followed by nausea and
headache
Occasionally skin reactions are severe
NVP is potentially hepatotoxic
Efavirenz
Side effects are headache, rashes, dizziness, insomnia and a variety of
neuropsychiatric symptoms
Contraindicated in pregnancy and in women likely to get pregnant, since
it is teratogenic
Because of its longer plasma t1⁄2, occasional missed doses of EFV are less
damaging
Cont.
39. Retroviral protease inhibitors (PIs)
Acts at a late step in HIV replication, i.e. Maturation of the new virus
particles when the RNA genome acquires the core proteins and enzymes
Bind to the active site of protease molecule, interfere with its cleaving
function, and are more effective viral inhibitors than AZT
Because they act at a late step of viral cycle, they are effective in both
newly as well as chronically infected cells
Nelfinavir, Lopinavir and Ritonavir induce their own metabolism
Patient acceptability and compliance are often low
Most prominent adverse effects of PIs are gastrointestinal intolerance,
headache, dizziness, limb and facial tingling, numbness and rashes
40. Lipodystrophy, dyslipidaemia and insulin resistance are of particular
concern
Diabetes may be exacerbated
Indinavir crystalises in urine and increases risk of urinary calculi
Atazanavir (ATV)
It is administered with light meal which improves absorption, while acid
suppressant drugs decrease its absorption
Bioavailability and efficacy of ATV is improved by combining with RTV
Dyslipidaemia and other metabolic complications are minimal with ATV
Jaundice occurs in some patients without liver damage due to inhibition
of hepatic glucuronyl transferase
Cont.
41. Entry (fusion) Inhibitor
Enfuvirtide
HIV derived synthetic peptide
Binds to HIV 1 envelope transmembrane glycoprotein (gp41) involved in
fusion of viral and cellular membranes
Entry of virus into host cell is blocked
Not active against HIV 2
Pharmacokinetics: administered s.c twice daily, used as add on drug in
earlier regimens
Adverse reactions: local nodule/ cyst at injection site
42. CCR5 receptor inhibitor
Maraviroc
Targets the host cell chemokine -CCR5 receptor and blocks it
Attachment and entry of virus is inhibited
Has no effect on CXCR4 receptor tropic HIV strains
Adverse reactions: impaired immune surveillance
Increased risk of infection/malignancy
43. Integrase Inhibitor
Raltegravir
Inhibits the viral enzyme integrase
HIV Integrase nicks the host chromosomal DNA and integrates the
proviral DNA with it
Active against both HIV 1 and 2 and causes improved CD4 cell count
Uses: As a component of initial triple drug regimen along with 2NRTIs
Adverse effect: Myopathy
HIV treatment principles and guidelines
44. Anti-Retroviral Combinations
Recommended by National AIDS control Organization
Preferred regimen:
1) Lamivudine + Zidovudine + Nevirapine
Alternative regimens:
1) Lamivudine + Zidovudine + Efavirenz
2) Lamivudine + Stavudine + Efavirenz
3) Lamivudine + Stavudine + Nevirapine
Other regimens:
1) Lamivudine + Tenofovir + Nevirapine
2) Lamivudine + Tenofovir + Efavirenz
3) Lamivudine + Zidovudine + Tenofovir
45. References
Goodman & Gilman “The Pharmacological Basis of Therapeutics” 12th
edition
Tripathi K.D. “Essentials of Medical Pharmacology” 7th edition 2013
Dr. TV Rao MD “Antiviral Drugs Basics” published in Health &
Medicine on Nov 17 2012