The document discusses various antiviral drugs, classifying them based on their mechanism of action and site of inhibition in the viral life cycle. It summarizes several representative antiviral drugs, including their chemistry, mechanism of action, antiviral spectrum, pharmacokinetics, administration, adverse effects and therapeutic uses. Key drugs discussed include amantadine, ribavirin, acyclovir, gancyclovir, vidarabine, idoxuridine and trifluridine.
The document discusses various antiviral drugs, classifying them based on their mechanism of action and the stage of the viral life cycle they target. It describes several nucleoside analog drugs like acyclovir, gancyclovir, vidarabine, idoxuridine and trifluridine which inhibit viral DNA polymerase after being phosphorylated. It also discusses mechanisms, spectra, pharmacokinetics and uses of specific antiviral drugs like amantadine, ribavirin, and protease inhibitors.
This document discusses various classes of antiviral drugs and examples within each class. It covers:
1) Agents for treating herpes simplex virus and varicella zoster virus like acyclovir which require phosphorylation to become activated.
2) Agents for treating cytomegalovirus like ganciclovir which is activated similarly to acyclovir but has different pharmacokinetics.
3) Antiretroviral agents used to treat HIV/AIDS that target different stages of the viral lifecycle such as reverse transcriptase inhibitors and protease inhibitors.
The document discusses anti-viral drugs, their mechanisms of action, spectra, pharmacokinetics and therapeutic uses. It describes how certain drugs like acyclovir are selectively activated within virus infected cells. Common classes include purine/pyrimidine analogs which inhibit viral DNA polymerase, and prodrugs requiring phosphorylation. Anti-virals inhibit active viral replication but do not eliminate non-replicating virus. Effective treatment depends on inhibitory drug concentrations at infection sites.
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 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.
Viruses are obligate intracellular parasites that contain genetic material enclosed in a protein coat. They replicate using host cell processes and lack cell structures. Antiviral drugs work by inhibiting virus development rather than destroying them. There are several classes of antiviral drugs that target different stages of the viral lifecycle, including reverse transcription, viral entry, assembly, and integration. Common antiviral drugs include nucleoside analogs, protease inhibitors, and integrase inhibitors. These drugs have varied mechanisms of action, pharmacokinetics, efficacy against different viruses, and potential adverse effects.
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 document discusses antiviral drugs used to treat various viral infections. It describes the classification of antiviral drugs, including drugs for herpes viruses like acyclovir and ganciclovir; influenza viruses like amantadine and zanamivir; hepatitis viruses like interferon and lamivudine; HIV like reverse transcriptase inhibitors, protease inhibitors, and fusion inhibitors. It provides details on the mechanisms of action, clinical uses, pharmacokinetics, and adverse effects of representative drugs in each class.
The document discusses various antiviral drugs, classifying them based on their mechanism of action and the stage of the viral life cycle they target. It describes several nucleoside analog drugs like acyclovir, gancyclovir, vidarabine, idoxuridine and trifluridine which inhibit viral DNA polymerase after being phosphorylated. It also discusses mechanisms, spectra, pharmacokinetics and uses of specific antiviral drugs like amantadine, ribavirin, and protease inhibitors.
This document discusses various classes of antiviral drugs and examples within each class. It covers:
1) Agents for treating herpes simplex virus and varicella zoster virus like acyclovir which require phosphorylation to become activated.
2) Agents for treating cytomegalovirus like ganciclovir which is activated similarly to acyclovir but has different pharmacokinetics.
3) Antiretroviral agents used to treat HIV/AIDS that target different stages of the viral lifecycle such as reverse transcriptase inhibitors and protease inhibitors.
The document discusses anti-viral drugs, their mechanisms of action, spectra, pharmacokinetics and therapeutic uses. It describes how certain drugs like acyclovir are selectively activated within virus infected cells. Common classes include purine/pyrimidine analogs which inhibit viral DNA polymerase, and prodrugs requiring phosphorylation. Anti-virals inhibit active viral replication but do not eliminate non-replicating virus. Effective treatment depends on inhibitory drug concentrations at infection sites.
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 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.
Viruses are obligate intracellular parasites that contain genetic material enclosed in a protein coat. They replicate using host cell processes and lack cell structures. Antiviral drugs work by inhibiting virus development rather than destroying them. There are several classes of antiviral drugs that target different stages of the viral lifecycle, including reverse transcription, viral entry, assembly, and integration. Common antiviral drugs include nucleoside analogs, protease inhibitors, and integrase inhibitors. These drugs have varied mechanisms of action, pharmacokinetics, efficacy against different viruses, and potential adverse effects.
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 document discusses antiviral drugs used to treat various viral infections. It describes the classification of antiviral drugs, including drugs for herpes viruses like acyclovir and ganciclovir; influenza viruses like amantadine and zanamivir; hepatitis viruses like interferon and lamivudine; HIV like reverse transcriptase inhibitors, protease inhibitors, and fusion inhibitors. It provides details on the mechanisms of action, clinical uses, pharmacokinetics, and adverse effects of representative drugs in each class.
This document summarizes various anti-viral and anti-fungal agents. It discusses the mechanism of action and clinical uses of nucleoside reverse transcriptase inhibitors like zidovudine, didanosine, lamivudine, emtricitabine and others for treating HIV. It also covers anti-herpes drugs like acyclovir, valacyclovir, famciclovir and penciclovir; anti-CMV drugs like ganciclovir and cidofovir; and other agents for treating hepatitis, influenza and fungal infections. The adverse effects and pharmacokinetics of many of these drugs are also summarized.
This document summarizes various anti-viral and anti-fungal agents. It discusses the mechanism of action and clinical uses of nucleoside reverse transcriptase inhibitors like zidovudine, didanosine, lamivudine, emtricitabine and others for treating HIV. It also covers anti-herpes drugs like acyclovir, valacyclovir, famciclovir and penciclovir; anti-CMV drugs like ganciclovir and cidofovir; and other agents for treating hepatitis, influenza and fungal infections. The adverse effects, pharmacokinetics and mechanisms of these different classes of drugs are summarized.
Most antiviral drugs target viral replication by interfering with viral nucleic acid synthesis or late protein synthesis. They require conversion to active triphosphate forms by host cell kinases to inhibit viral polymerases more selectively than host polymerases. Combination antiviral therapy increases effectiveness and delays drug resistance emergence. Current HIV treatment involves two or three drugs before symptoms, often two reverse transcriptase inhibitors plus a protease inhibitor to slow viral load increases and delay resistance.
Most antiviral drugs target viral replication by interfering with viral nucleic acid synthesis or late protein synthesis. They require conversion to active triphosphate forms by host cell kinases to inhibit viral polymerases more selectively than host polymerases. Combination antiviral therapy increases effectiveness and delays drug resistance emergence. Current HIV treatment involves two or three drugs before symptoms, often two reverse transcriptase inhibitors plus a protease inhibitor to slow viral load increases and delay resistance.
This document discusses antiviral agents for nonretrovirals. It begins by outlining the key learning objectives which are to describe viral infections, classification of antiviral agents, their mechanisms of action and resistance. It then classifies antiviral agents into non-retroviral and antiretroviral categories. Under non-retroviral agents, it describes treatments for influenza, herpes and hepatitis viruses. It provides details on specific drugs for each virus type, including their mechanisms of action, resistance and pharmacokinetics.
The document discusses various antiviral agents, their mechanisms of action, dosages, and side effects. It covers agents for coronaviruses like remdesivir, monoclonal antibodies, favipiravir, and tocilizumab. It also discusses acyclovir and related agents for herpes viruses, ganciclovir for CMV, foscarnet, and cidofovir. Finally, it summarizes oseltamivir and zanamivir for influenza viruses. The document provides detailed information on the pharmacology of different classes of antiviral drugs.
This document discusses antiviral drugs used to treat retrovirus infections such as HIV. It classifies antiretroviral drugs into different categories based on their mechanism of action, including nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors, CCR5 receptor inhibitors, and integrase inhibitors. Key drugs from each category are described in terms of their pharmacological properties and clinical applications. The principles of highly active antiretroviral therapy and guidelines for HIV treatment and prevention are also summarized.
This document discusses various antiviral drugs that target different stages of the viral lifecycle. It describes the mechanism of action, pharmacokinetics, uses, and side effects of several nucleoside analogues (acyclovir, cidofovir, famciclovir, ganciclovir), nucleotide analogues (foscarnet, ribavirin), and antisense oligonucleotides (fomivirsen) used to treat infections caused by DNA and RNA viruses like herpesviruses, influenza, hepatitis, and cytomegalovirus. The drugs inhibit viral DNA or RNA synthesis through competitive inhibition or chain termination mechanisms. Many require activation by viral or host kinases to form active triphosphate
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.
Antiviral drugs act by inhibiting viral replication without severely affecting host cells. Current antivirals target viruses like herpes, hepatitis, HIV, influenza, and RSV. They work by inhibiting viral absorption, nucleic acid synthesis, or protein synthesis. Anti-herpes drugs like acyclovir are selectively activated within infected cells. Antiretrovirals include reverse transcriptase inhibitors and protease inhibitors. Interferons stimulate antiviral defenses. Antivirals are used to treat associated viral infections and diseases while managing resistance.
This document provides an overview of HIV/AIDS, including:
- HIV is caused by the human immunodeficiency virus (HIV) which is a retrovirus.
- As of 2016, there were approximately 36.7 million people living with HIV globally.
- HIV diagnosis involves ELISA and Western blot tests to detect HIV antibodies and viral proteins.
- HIV treatment involves the use of antiretroviral drugs from several classes including nucleoside/nucleotide reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors, CCR5 co-receptor antagonists, and integrase inhibitors.
- Co-infections with tuberculosis require specialized treatment reg
The document discusses several antiviral and antifungal agents, their mechanisms of action, clinical uses, and side effects. It covers agents that target herpes viruses like acyclovir and famciclovir, cytomegalovirus like ganciclovir and cidofovir, and influenza like amantadine and rimantadine. The agents work by inhibiting viral entry, replication, or incorporation into viral DNA. They are used to treat herpes, CMV, influenza and other viral infections. Common side effects include gastrointestinal issues, renal toxicity, and myelosuppression.
The document discusses several antiviral and antifungal agents, their mechanisms of action, clinical uses, and side effects. It covers agents that target herpes viruses like acyclovir and famciclovir, cytomegalovirus like ganciclovir and cidofovir, and influenza like amantadine and rimantadine. The agents work by inhibiting viral entry, replication, or incorporation into viral DNA. They are used to treat herpes, CMV, influenza and other viral infections. Common side effects include gastrointestinal issues, renal toxicity, and myelosuppression.
anti virals -medication used against viral actionTeena42750
This document discusses antiviral drugs and classifies them based on their mechanism of action and target viruses. It describes several classes of antiviral drugs including anti-herpes drugs like acyclovir and famciclovir, anti-influenza drugs like oseltamivir and zanamivir, and various classes of antiretroviral drugs used to treat HIV like nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and entry inhibitors. Each drug is discussed in terms of its mechanism of action, target virus, uses, and common side effects.
This document discusses antiviral drugs used to treat various viral infections. It begins by explaining the characteristics of viruses and stages of viral replication. It then categorizes and describes antiviral drugs for herpes, influenza, hepatitis B and C viruses. The drugs discussed include acyclovir, ganciclovir, amantadine, ribavirin, interferons, entecavir, tenofovir and newer oral antivirals for hepatitis C. The mechanisms of action, spectra, pharmacokinetics and therapeutic uses of these drugs are summarized. Adverse effects and importance of drug resistance are also mentioned.
This document discusses various classes of antiviral drugs, including their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects. It describes DNA and RNA polymerase inhibitors such as acyclovir, ganciclovir, and ribavirin which work by inhibiting viral replication. It also covers adamantane derivatives amantadine and rimantidine which inhibit influenza virus uncoating, as well as neuraminidase inhibitors oseltamivir and zanamivir which prevent viral spread. Immunomodulators like interferons are also summarized, which activate the immune system against viruses.
This document discusses various classes of antiviral drugs, including those that target herpes viruses, influenza virus, hepatitis viruses, and HIV. It provides details on the mechanism of action, pharmacokinetics, uses, and adverse effects of representative drugs in each class, such as acyclovir for herpes, amantadine/rimantadine for influenza, lamivudine/adefovir for hepatitis B, ribavirin/interferon for hepatitis C, and zidovudine as the prototype nucleoside reverse transcriptase inhibitor for HIV. The goal of antiviral treatment is to inhibit virus-specific replication events while minimizing effects on host cell processes.
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
This document summarizes various anti-viral and anti-fungal agents. It discusses the mechanism of action and clinical uses of nucleoside reverse transcriptase inhibitors like zidovudine, didanosine, lamivudine, emtricitabine and others for treating HIV. It also covers anti-herpes drugs like acyclovir, valacyclovir, famciclovir and penciclovir; anti-CMV drugs like ganciclovir and cidofovir; and other agents for treating hepatitis, influenza and fungal infections. The adverse effects and pharmacokinetics of many of these drugs are also summarized.
This document summarizes various anti-viral and anti-fungal agents. It discusses the mechanism of action and clinical uses of nucleoside reverse transcriptase inhibitors like zidovudine, didanosine, lamivudine, emtricitabine and others for treating HIV. It also covers anti-herpes drugs like acyclovir, valacyclovir, famciclovir and penciclovir; anti-CMV drugs like ganciclovir and cidofovir; and other agents for treating hepatitis, influenza and fungal infections. The adverse effects, pharmacokinetics and mechanisms of these different classes of drugs are summarized.
Most antiviral drugs target viral replication by interfering with viral nucleic acid synthesis or late protein synthesis. They require conversion to active triphosphate forms by host cell kinases to inhibit viral polymerases more selectively than host polymerases. Combination antiviral therapy increases effectiveness and delays drug resistance emergence. Current HIV treatment involves two or three drugs before symptoms, often two reverse transcriptase inhibitors plus a protease inhibitor to slow viral load increases and delay resistance.
Most antiviral drugs target viral replication by interfering with viral nucleic acid synthesis or late protein synthesis. They require conversion to active triphosphate forms by host cell kinases to inhibit viral polymerases more selectively than host polymerases. Combination antiviral therapy increases effectiveness and delays drug resistance emergence. Current HIV treatment involves two or three drugs before symptoms, often two reverse transcriptase inhibitors plus a protease inhibitor to slow viral load increases and delay resistance.
This document discusses antiviral agents for nonretrovirals. It begins by outlining the key learning objectives which are to describe viral infections, classification of antiviral agents, their mechanisms of action and resistance. It then classifies antiviral agents into non-retroviral and antiretroviral categories. Under non-retroviral agents, it describes treatments for influenza, herpes and hepatitis viruses. It provides details on specific drugs for each virus type, including their mechanisms of action, resistance and pharmacokinetics.
The document discusses various antiviral agents, their mechanisms of action, dosages, and side effects. It covers agents for coronaviruses like remdesivir, monoclonal antibodies, favipiravir, and tocilizumab. It also discusses acyclovir and related agents for herpes viruses, ganciclovir for CMV, foscarnet, and cidofovir. Finally, it summarizes oseltamivir and zanamivir for influenza viruses. The document provides detailed information on the pharmacology of different classes of antiviral drugs.
This document discusses antiviral drugs used to treat retrovirus infections such as HIV. It classifies antiretroviral drugs into different categories based on their mechanism of action, including nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors, CCR5 receptor inhibitors, and integrase inhibitors. Key drugs from each category are described in terms of their pharmacological properties and clinical applications. The principles of highly active antiretroviral therapy and guidelines for HIV treatment and prevention are also summarized.
This document discusses various antiviral drugs that target different stages of the viral lifecycle. It describes the mechanism of action, pharmacokinetics, uses, and side effects of several nucleoside analogues (acyclovir, cidofovir, famciclovir, ganciclovir), nucleotide analogues (foscarnet, ribavirin), and antisense oligonucleotides (fomivirsen) used to treat infections caused by DNA and RNA viruses like herpesviruses, influenza, hepatitis, and cytomegalovirus. The drugs inhibit viral DNA or RNA synthesis through competitive inhibition or chain termination mechanisms. Many require activation by viral or host kinases to form active triphosphate
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.
Antiviral drugs act by inhibiting viral replication without severely affecting host cells. Current antivirals target viruses like herpes, hepatitis, HIV, influenza, and RSV. They work by inhibiting viral absorption, nucleic acid synthesis, or protein synthesis. Anti-herpes drugs like acyclovir are selectively activated within infected cells. Antiretrovirals include reverse transcriptase inhibitors and protease inhibitors. Interferons stimulate antiviral defenses. Antivirals are used to treat associated viral infections and diseases while managing resistance.
This document provides an overview of HIV/AIDS, including:
- HIV is caused by the human immunodeficiency virus (HIV) which is a retrovirus.
- As of 2016, there were approximately 36.7 million people living with HIV globally.
- HIV diagnosis involves ELISA and Western blot tests to detect HIV antibodies and viral proteins.
- HIV treatment involves the use of antiretroviral drugs from several classes including nucleoside/nucleotide reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, fusion inhibitors, CCR5 co-receptor antagonists, and integrase inhibitors.
- Co-infections with tuberculosis require specialized treatment reg
The document discusses several antiviral and antifungal agents, their mechanisms of action, clinical uses, and side effects. It covers agents that target herpes viruses like acyclovir and famciclovir, cytomegalovirus like ganciclovir and cidofovir, and influenza like amantadine and rimantadine. The agents work by inhibiting viral entry, replication, or incorporation into viral DNA. They are used to treat herpes, CMV, influenza and other viral infections. Common side effects include gastrointestinal issues, renal toxicity, and myelosuppression.
The document discusses several antiviral and antifungal agents, their mechanisms of action, clinical uses, and side effects. It covers agents that target herpes viruses like acyclovir and famciclovir, cytomegalovirus like ganciclovir and cidofovir, and influenza like amantadine and rimantadine. The agents work by inhibiting viral entry, replication, or incorporation into viral DNA. They are used to treat herpes, CMV, influenza and other viral infections. Common side effects include gastrointestinal issues, renal toxicity, and myelosuppression.
anti virals -medication used against viral actionTeena42750
This document discusses antiviral drugs and classifies them based on their mechanism of action and target viruses. It describes several classes of antiviral drugs including anti-herpes drugs like acyclovir and famciclovir, anti-influenza drugs like oseltamivir and zanamivir, and various classes of antiretroviral drugs used to treat HIV like nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, protease inhibitors, and entry inhibitors. Each drug is discussed in terms of its mechanism of action, target virus, uses, and common side effects.
This document discusses antiviral drugs used to treat various viral infections. It begins by explaining the characteristics of viruses and stages of viral replication. It then categorizes and describes antiviral drugs for herpes, influenza, hepatitis B and C viruses. The drugs discussed include acyclovir, ganciclovir, amantadine, ribavirin, interferons, entecavir, tenofovir and newer oral antivirals for hepatitis C. The mechanisms of action, spectra, pharmacokinetics and therapeutic uses of these drugs are summarized. Adverse effects and importance of drug resistance are also mentioned.
This document discusses various classes of antiviral drugs, including their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects. It describes DNA and RNA polymerase inhibitors such as acyclovir, ganciclovir, and ribavirin which work by inhibiting viral replication. It also covers adamantane derivatives amantadine and rimantidine which inhibit influenza virus uncoating, as well as neuraminidase inhibitors oseltamivir and zanamivir which prevent viral spread. Immunomodulators like interferons are also summarized, which activate the immune system against viruses.
This document discusses various classes of antiviral drugs, including those that target herpes viruses, influenza virus, hepatitis viruses, and HIV. It provides details on the mechanism of action, pharmacokinetics, uses, and adverse effects of representative drugs in each class, such as acyclovir for herpes, amantadine/rimantadine for influenza, lamivudine/adefovir for hepatitis B, ribavirin/interferon for hepatitis C, and zidovudine as the prototype nucleoside reverse transcriptase inhibitor for HIV. The goal of antiviral treatment is to inhibit virus-specific replication events while minimizing effects on host cell processes.
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
Among the factors that lead to the occurrence of gastrointestinal infections are the hygienic and sanitary deficiencies that characterize our markets and other places where raw or cooked food is sold, poor environmental sanitation in communities, deficiencies in water treatment (or in the process of its plumbing), risky hygienic-sanitary habits (not washing hands after major and/or minor needs), among others.
These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
To prevent this, it is necessary to promote health education, improve the hygienic-sanitary conditions of markets and communities in general as a way of promoting, preserving and prolonging PUBLIC HEALTH.
Gastritis and Gastric Health
Gastric Health is one of the most relevant concerns in human health, with gastrointestinal infections being among the main illnesses that affect humans.
Among gastric problems, we have GASTRITIS AND GASTRIC ULCERS as the main public health problems. Gastritis and gastric ulcers normally result from inflammation and corrosion of the walls of the stomach (gastric mucosa) and are generally associated (caused) by the bacterium Helicobacter pylor, which, according to the literature, this bacterium settles on these walls (of the stomach) and starts to release urease that ends up altering the normal pH of the stomach (acid), which leads to inflammation and corrosion of the mucous membranes and consequent gastritis or ulcers, respectively.
In addition to bacterial infections, gastritis and gastric ulcers are associated with several factors, with emphasis on prolonged fasting, chemical substances including drugs, alcohol, foods with strong seasonings including chilli, which ends up causing inflammation of the stomach walls and/or corrosion. of the same, resulting in the appearance of wounds and consequent gastritis or ulcers, respectively.
Among patients with gastritis and/or ulcers, one of the dilemmas is associated with the foods to consume in order to minimize the sensation of pain and discomfort.
Dr. Tan's Balance Method.pdf (From Academy of Oriental Medicine at Austin)GeorgeKieling1
Home
Organization
Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
About AOMA: The Academy of Oriental Medicine at Austin offers a masters-level graduate program in acupuncture and Oriental medicine, preparing its students for careers as skilled, professional practitioners. AOMA is known for its internationally recognized faculty, award-winning student clinical internship program, and herbal medicine program. Since its founding in 1993, AOMA has grown rapidly in size and reputation, drawing students from around the nation and faculty from around the world. AOMA also conducts more than 20,000 patient visits annually in its student and professional clinics. AOMA collaborates with Western healthcare institutions including the Seton Family of Hospitals, and gives back to the community through partnerships with nonprofit organizations and by providing free and reduced price treatments to people who cannot afford them. The Academy of Oriental Medicine at Austin is located at 2700 West Anderson Lane. AOMA also serves patients and retail customers at its south Austin location, 4701 West Gate Blvd. For more information see www.aoma.edu or call 512-492-303434.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Discover the benefits of homeopathic medicine for irregular periods with our guide on 5 common remedies. Learn how these natural treatments can help regulate menstrual cycles and improve overall menstrual health.
Visit Us: https://drdeepikashomeopathy.com/service/irregular-periods-treatment/
19. Replicative cycles of herpes simplex virus, an example of a DNA virus,
and the probable sites of action of antiviral agents.
20. Replicative cycles of influenza, an example of an RNA virus, and
the loci for effects of antiviral agents.
21. ANTIVIRAL DRUGS: GENERAL FEATURES
- Many antiviral drugs are purine or pyrimidine analogs.
-Many antiviral drugs are prodrugs.
They must be phosphorylated by viral or cellular enzymes in order to
become active.
- Antiviral drugs typically have a restricted spectrum of antiviral activity
and inhibit a specific viral protein, most often an enzyme involved in
viral nucleic acid synthesis.
- Single nucleotide changes leading to critical amino acid substitutions in
a target protein often are sufficient to cause antiviral drug resistance.
- Current agents inhibit active replication but do not eliminate
nonreplicating or latent viruses so that viral growth may resume after
drug removal. Effective host immune response remain essential for
recovery from infection.
22. - Antiviral drugs may have antiviral synergistic effects when given
concomitantly (i.e. gancyclovir and foscarnet, zidovudine and
didanosine, zidovudine and protease inhibitors, etc.). In other cases
toxic synergistic effects preclude concurrent administration of two
antiviral drugs (i.e. zidovudine and acyclovir, zidovudine and
gancyclovir, etc.)
- Clinical efficacy of antiviral drugs depends on achieving
inhibitory concentrations within infected cells. Therefore a clear
relationship between blood concentration and clinical response
have not been established for most antiviral agents.
23. PHARMACOLOGY OF AMANTADINE AND CONGENERS
Chemistry
-Amantadine and rimantadine are tricyclic amines.
Mechanism of action
-Inhibition of viral uncoating by:
a) Blockade of the viral membrane matrix protein M2, which function as an ion
channel. This channel is required for the fusion of the viral membrane with the
cell membrane.
b) Rising the pH of the endosome (an acidic pH inside the endosome is required
for viral uncoating)
Antiviral spectrum and resistance
-Influenza A virus (not B and C virus)
-Resistant variants are selected rapidly during treatment (approximately in 30% of
treated patients)
Other effects
-Amantadine has antiparkinsonian effects. The mechanism of action is not clear
but it may be related to:
a) the antimuscarinic properties of the drug
b) the stimulation of the synthesis and release of dopamine (and other
catecholamines)
24.
25. Pharmacokinetics and administration (amantadine)
-F(oral): 50-90%
-Distribution in all body tissues including CNS
-Renal excretion: > 90%
-Half lives: » 16 hours
-Administration: oral
Adverse effects
-Anorexia, nausea and vomiting ,stypsis, xerostomia, urinary retention.
-Nervousness ,insomnia, lightheadedness, difficulty concentrating, ataxia
-Delirium, hallucinations, seizures (with high doses)
-Teratogenic effects in animals
Therapeutic uses
-Treatment of influenza A (treatment within the first 48 hours after the exposure
reduces the duration of symptoms and speeds functional recovery)
-Prevention of influenza A (70-90% protective). The
drugs do not impair the immune response to influenza A vaccine.
26. PHARMACOLOGY OF RIBAVIRIN
Chemistry
-Ribavirin is a purine nucleoside analog.
Mechanism of action
-Inhibition of synthesis of guanosine-triphosphate which leads to
inhibition of nucleic acid synthesis in general
-Specific inhibition of viral mRNA synthesis
Antiviral spectrum and resistance
-Wide range of DNA and RNA viruses are susceptible, including
influenza A, B and C viruses, parainfluenza viruses, measles virus,
HSV-1, HSV-2, CMV, RSV
-Emergence of viral resistance to ribavirin has not been documented.
27.
28. Pharmacokinetics and administration
-F(oral): 50-90% ; F(aerosol) < 5%
-Distribution in all body tissues, except CNS
-Renal excretion: » 35%
-Half lives: » 30 hours
-Administration: oral, IV, inhalatory
Adverse effects
When given by aerosol:
-Conjunctival irritation, transient wheezing, reversible deterioration in pulmonary
function.
When given orally or IV:
-Dose-dependent hemolytic anemia and bone marrow suppression
-Headache, insomnia, mood alteration
-Teratogenic effects in animals
Therapeutic uses
Ribavirin is the drug of choice for:
-RSV bronchiolitis and pneumonia in hospitalized children (given by aerosol)
-Lassa fever
Ribavirin is an alternative drug for:
-Influenza, parainfluenza, measles virus infection in immunocompromised patients
29. PHARMACOLOGY OF ACYCLOVIR AND CONGENERS
Chemistry
-Acyclovir, gancyclovir, famcyclovir, pemcyclovir all are guanine
nucleoside analogs.
Mechanism of action
-All drugs are phosphorylated by a viral thymidine-kinase, then
metabolized by host cell kinases to nucleotide analogs.
-The analog inhibits viral DNA-polymerase
-Only actively replicating viruses are inhibited
Antiviral spectrum and resistance
-Acyclovir: HSV-1, HSV-2, VZV.
-Gancyclovir: HSV-1, HSV-2, VZV, EBV, CMV.
-Viral resistance may occur and may be due to:
a) decreased production of thymidine kinase
b) altered thymidine kinase substrate specificity
c) altered viral DNA polymerase
32. Pharmacokinetics and administration
-F(oral): acyclovir 20-30%; gancyclovir < 10%
-Distribution in all body tissues including CNS
(CSF/plasma ratio » 0.5)
-Renal excretion: > 80%
-Half lives: 2-5 hours
-Administration: topical, oral (acyclovir), IV (acyclovir, gancyclovir)
Adverse effects
-Nausea and vomiting ,diarrhea (acyclovir PO)
-Neurotoxicity (1-5% of patients) (headache, tremor, behavioral changes, delirium,
seizures, coma) (acylovir and gancyclovir, high doses IV)
-Nephrotoxicity (crystalluria, hematuria, renal insufficiency (acyclovir, high doses IV)
-Mielosuppression (neutropenia, thrombocytopenia) (gancyclovir)
-Teratogenic effects in animals
Therapeutic uses
Acyclovir is the drug of choice for:
-Genital HSV infections
-HSV encephalitis
-HSV infections in immunocompromised patient Gancyclovir is the drug of choice for:
-CMV retinitis in immunocompromised patient
-Prevention of CMV disease in transplant patients
33. PHARMACOLOGY OF VIDARABINE
Chemistry
-Vidarabine is an adenine nucleoside analog.
Mechanism of action
-The drug is converted by cellular enzymes to its triphosphate analog
which inhibits viral (and, to a lesser extent, human) DNA-polymerase.
Antiviral spectrum and resistance
-Antiviral spectrum of vidarabine includes HSV-1,
HSV-2 and VZV.
-Resistant variants due to mutation in DNA-polymerase have been
detected.
-Cross-resistance between vidarabine and other antiviral drugs is rare.
34.
35. Pharmacokinetics and administration
-F(oral): < 2%
-Distribution in all body tissues including CNS
-Renal excretion: > 50%
-Half life: 3-4 hours
-Administration: topical or IV.
Adverse effects
Dose-dependent toxicity (after IV administration):
-Neurotoxicity (headache, tremor, confusion, seizures)
-Anemia, leukopenia, thrombocytopenia.
-Syndrome of inappropriate secretion of ADH.
-The drug is mutagenic and teratogenic in animals.
Therapeutic uses
Vidarabine is an alternative drug for:
-HSV keratoconjunctivitis (topical).
-Neonatal herpes.
-VZV infections in immunocompromised patient.
36. PHARMACOLOGY OF IDOXURIDINE AND TRIFLURIDINE
Chemistry
-Idoxuridine and trifluridine are pyrimidine nucleoside analogs.
Mechanism of action
-The drugs are converted by cellular enzymes to their triphosphate analogs
which inhibits viral (and, to a lesser extent, human) DNA synthesis.
Antiviral spectrum and resistance
-Antiviral spectrum includes HSV-1, HSV-2 and VZV.
-Prolonged treatment can select drug-resistant mutants.
Administration
-topically administered (eye, oral, genital mucosae)
Adverse effects
-Pain, pruritus, edema involving the eye or lids.
-Allergic reactions (rare)
Therapeutic uses
-Ocular, oral, genital HSV infections
37.
38. PHARMACOLOGY OF FOSCARNET
Chemistry
-Foscarnet is an inorganic pyrophosphate analog
Mechanism of action
-The drug directly inhibits viral DNA-polymerase and viral inverse
transcriptase (it does not require phosphorylation for antiviral
activity)
Antiviral spectrum and resistance
-Antiviral spectrum of foscarnet includes HSV-1, HSV-2, VZV,
CMV and HIV.
-Resistance may be due to altered viral DNA polymerase
-Cross-resistance between foscarnet and other antiviral drugs is very
rare.
39.
40. Pharmacokinetics and administration
-F(oral): 10-20%
-Distribution in all body tissues including CNS (CSF/plasma ratio » 0.7)
-Renal excretion: > 80%
-Half life: 3-4 days
-Administration: IV
Adverse effects
-Hypocalcemia and hypomagnesemia (due to chelation of the drug with
divalent cations) are common.
-Neurotoxicity (headache, tremor, irritability, hallucinations, seizures)
-Nephrotoxicity (acute tubular nephrosis, interstitial nephritis)
Therapeutic uses
Foscarnet is an alternative drug for
-HSV infections (due to thymidine kinase deficient strains which are
acyclovir resistant)
-HSV infections in immunocompromised patient
-CMV retinitis (gancyclovir resistant)
-CMV infections in immunocompromised patient
41. Replicative cycle of HIV-1, an example of a retrovirus, showing the sites
of action of antiviral agents.
Various antiviral agents are shown in blue. Key: RT, reverse
transcriptase; cDNA, complementary DNA; mRNA, messenger RNA; Tat, a
protein that regulates viral transcription and affects the rate of
replication; RNaseH, ribonuclease H; gp120, envelope glycoprotein.
43. PHARMACOLOGY OF ZIDOVUDINE
Chemistry
-Zidovudine is a thymine nucleoside analog (deoxythymidine)
Mechanism of action
-The drug is phosphorylated by cellular thymidine kinase to the corresponding
nucleotide analog
-The analog inhibits the RNA dependent DNA-polymerase (inverse
transcriptase) so blocking DNA synthesis
-Viral DNA-polymerases are more sensitive to this inhibition than are
mammalian polymerases
Antiviral spectrum and resistance
-Antiviral spectrum includes HIV-1, HIV-2, HTLV-1 and other retroviruses.
-Highly resistant mutants have been recovered from many AIDS patients
treated for more than 6 months.
44.
45. Pharmacokinetics
-F(oral): » 65%
-Distribution in all body tissues including CNS (CSF/plasma ratio » 0.5)
-Biotransformation: » 85% (glucuronidation)
-Renal excretion: » 15%
-Half life: » 1 hour
Adverse effects
-Severe anemia and leukopenia, due to bone marrow suppression (30% of patients
need transfusions)
-Malaise, fever, fatigue, headache, nausea and vomiting, diarrhea, insomnia,
agitation (mainly during first few weeks)
-Myopathy (10% of patients after long term use)
-Encephalopathy (confusion, tremulousness), seizures (with high doses, can be fatal)
-Hepatic steatosis, lactic acidosis (can be fatal)
[toxicity is increased by concomitant use of drugs which inhibit glucuronidation (e.g
fluconazole, cimetidine) or are extensively gucuronosylconjugated (e.g.
benzodiazepines)]
Therapeutic uses
-Initial drug of choice in AIDS patients with CD4 counts less than 500/mm3. (the
drug initially reduces morbidity and mortality, but the effect is transient)
-In asymptomatic HIV-infected individuals the drug slow the rate of progression of
AIDS.
46. PHARMACOLOGY OF OTHER DEOXYNUCLEOSIDES USED IN
AIDS
Chemistry
-Didanosine is a purine deoxynucleoside .
-Zalcitabine and stavudine are pyrimidine deoxynucleosides.
Mechanism of action
-The drug are phosphorylated by cellular kinases to the corresponding
nucleotide analogs.
-The analog inhibits the RNA dependent DNA-polymerase (inverse
transcriptase) so blocking DNA synthesis
-Viral DNA-polymerases are more sensitive to this inhibition than are
mammalian polymerases
Antiviral spectrum and resistance
-The drugs are active against HIV-1 and HIV-2, including most zidovudine
resistant strains.
-Resistant mutants have been recovered from treated patients.
47.
48. Pharmacokinetics
-F(oral): variable (didanosine »40%; zalcitabine >80%)
-Distribution in all body tissues including CNS
-Renal excretion: 40-75%
-Half lives: 1-3 hours
Adverse effects
-Painful peripheral neuropathy (up to 30% of patients)
-Pancreatitis (can be fatal)
-Headache, insomnia, agitation, seizures (didanosine)
-Arthralgia, fever, rash
-Stomatitis, esophageal ulceration (zalcitabine)
-Hepatic steatosis, lactic acidosis (can be fatal)
Therapeutic uses
-Advanced HIV infection in patients who are intolerant of or deteriorating on
zidovudine.
49. PHARMACOLOGY OF HIV PROTEASE INHIBITORS
Chemistry
-Atazanavir, Darunavir, Fosamprenavir, Lopinavir, Nelfinavir, Tipranavir,
Saquinavir, Ritonavir and Indinavir are structural analogs of HIV protease
Mechanism of action
-HIV protease is an aspartic endopeptidase that cleaves viral polypeptide
products to form structural proteins of the virion core and essential viral
enzymes (i.e reverse transcriptase, integrase, etc.)
-By inhibiting HIV protease the drugs block the maturation of the virus and
therefore are active in both acutely and chronically infected cells
-The drugs are highly specific inhibitors of HIV protease and do not affect
human endopeptidases
Antiviral spectrum and resistance
-The drugs are active against HIV-1 and HIV-2, including most strains
resistant to nucleoside analogs -Resistant mutants have emerged during
therapy.
-Some cross-resistance occurs among HIV protease inhibitors, but not with
other antiviral drugs.
50. Pharmacokinetics and administration
-F(oral): 4-10% (due to extensive first pass-effect)
-Distribution in all body tissues, except CNS
-Biotransformation: extensive, by the mixed function oxidase system, in
intestinal wall and liver.
-Administration: PO
Adverse effects
-Nausea and vomiting, diarrhea, abdominal pain
-Stomatitis, glossitis, gastritis, hemorrhoids, pancreatitis (rare)
-Elevated hepatic aminotransferase levels, hepatitis, jaundice (rare)
-Skin rashes, urticaria
-Stevens-Johnson syndrome (very rare)
-Anemia, leukopenia, thrombocytopenia (rare)
Drug interactions
-Drugs which inhibit the hepatic mixed function oxidase system may increase
plasma concentrations of HIV protease inhibitors.
Therapeutic uses
-Advanced HIV infection (in combination with deoxynucleoside antiretroviral
drugs)
51.
52. Entry Inhibitors
Efuvirtide (T-20)
36-amino acid peptide binds to gp41 viral envelope glycoprotein
Resistance can occur but there is no cross resistance
Drug administration subcutaneously in combination with other
antiretroviral drugs
Side effects: Local injection site reaction, hypersensitivity
reaction,Eosinophilia
Maraviroc
binds specifically and selectively to CCR5
55. PHARMACOLOGY OF INTERFERONS
Chemistry
-Interferons are inducible endogenous cytokines (glycoproteins)
-Three major classes of human interferons (IFN) are:
IFN-alpha (human leukocyte IFN), induced by viruses
IFN-beta (human fibroblast IFN), induced by viruses
IFN-gamma (human immune IFN), induced by antigens
Mechanism of antiviral action
-Binding to specific receptors of the host cells
-Induction of the following main enzymes:
1) a protein kinase which inhibits protein synthesis
2) an oligoadenylate synthase which leads to degradation of viral mRNA
3) a phosphodiesterase which can inhibit tRNA
-The action of these enzymes leads to an inhibition of translation (late viral
RNA and protein synthesis)
Antiviral spectrum
-Antiviral spectrum includes HBV, HCV, HDV, HSV, VZV, CMV and human
papillomavirus (HPV).
Other effects
-Interferons possess immunomodulating and antiproliferative actions and may
inhibit the growth of certain cancer cells.
56.
57. Pharmacokinetics
-F(oral): < 1% ;
-F(IM, SC): IFN-alpha > 80% ; IFN-beta » 40%
-Distribution in all body tissues, except CNS and eye.
-Half lives: 1-4 hours
Adverse effects
-Acute flu-like syndrome (fever, headache, myalgia, arthralgia, nausea and vomiting)
-Bone marrow suppression (granulocytopenia, thrombocytopenia)
-Neurotoxicity (fatigue, sleepiness, confusion, seizures) (after high doses)
-Cardiotoxicity (cardiac failure)(after high doses)
-Hepatotoxicity (after high doses)
-Interstitial nephritis (after high doses)
-Hypersensitivity reactions (rare)
-Impairment of fertility
Therapeutic uses
-Chronic hepatitis B and C (improvement in 25-50% of patients. Administration usually
last 4-6 months. Remission may be sustained, but complete disappearance is seen only in
30% of cases)
-HZV infection in cancer patients (to prevent the dissemination of the infection)
-CMV infections in renal transplant patients
-Refractory condylomata acuminata (given by intralesional injection. Complete clearance
is seen in 36-62% of patients)
-Hairy cell leukemia (in combination with zidovudine)
-AIDS related Kaposi’s sarcoma