SMV 242 LECTURE NOTE

Sample questions

1. HIV and AIDS

Question: What is HIV, and how does it cause AIDS? Name two ways HIV can
spread and one treatment to manage it.

Answer:
HIV (Human Immunodeficiency Virus) is a virus that attacks the body’s
immune system, especially CD4+ T-cells, which help fight infections. Over
time, HIV destroys these cells, weakening the immune system and leading to
AIDS (Acquired Immunodeficiency Syndrome), where the body can’t fight
infections or cancers.

 Spread: HIV spreads through sexual contact (e.g., unprotected sex)

and sharing needles with infected blood.

 Treatment: Antiretroviral therapy (ART) uses drugs to lower the virus

amount in the body and keep the immune system strong.

2. Hepatitis Viruses

Question: What are the main differences between Hepatitis A and Hepatitis B
in how they spread and their effects on the body? Name one treatment or
prevention method for each.

Answer:

 Hepatitis A (HAV): Spreads through contaminated food or water (fecal-

oral route). It causes short-term liver inflammation (acute hepatitis)
with symptoms like fever and jaundice but usually doesn’t cause long-
term damage.

 Prevention: HAV vaccine.

 Hepatitis B (HBV): Spreads through blood, sexual contact, or from

mother to baby. It can cause acute or chronic liver disease,
sometimes leading to liver damage or cancer.

 Treatment: Antiviral drugs like tenofovir or a vaccine to

prevent infection.

3. Herpesviruses

Question: What is a herpesvirus, and how does it stay in the body? Give one
example of a herpesvirus and a disease it causes, plus one way to treat it.

Answer:
A herpesvirus is a virus that causes infections and stays in the body
forever in a “sleeping” state called latency, hiding in cells like nerves
or immune cells. It can “wake up” and cause symptoms.

 Example: Herpes Simplex Virus (HSV-1) causes cold sores (painful

sores around the mouth).

 Treatment: Antiviral drugs like acyclovir reduce symptoms but don’t

cure the virus.
Viral Diseases I: HIV, Hepatitis Viruses,
Herpesviruses
1. HIV (Human Immunodeficiency Virus)
Causative Agent:
Human Immunodeficiency Virus (HIV), a retrovirus from the genus Lentivirus, family Retroviridae.
Two main types: HIV-1 (most common globally) and HIV-2 (primarily West Africa).
History/Origin:
HIV likely originated from zoonotic transmission of simian immunodeficiency viruses (SIV) from
non-human primates in Central Africa. HIV-1 is linked to chimpanzees, and HIV-2 to sooty
mangabeys. Earliest confirmed case traces to 1959 in the Democratic Republic of Congo. AIDS
(Acquired Immunodeficiency Syndrome) was recognized in the early 1980s in the U.S.
Classification:
Family: Retroviridae
Genus: Lentivirus
Types: HIV-1 (groups M, N, O, P) and HIV-2.
Biology:
HIV is an enveloped, single-stranded RNA virus with reverse transcriptase, which converts RNA to
DNA for integration into host cell genomes. It primarily targets CD4+ T-cells, macrophages, and
dendritic cells. The virus has a lipid envelope with gp120 and gp41 glycoproteins for cell entry.
Mode of Transmission:
Sexual contact (vaginal, anal, oral; especially high-risk in unprotected anal sex).
Bloodborne (sharing needles, transfusions with contaminated blood).
Vertical (mother-to-child during pregnancy, childbirth, or breastfeeding).
Rarely through occupational exposure (e.g., needlestick injuries).
Pathogenesis:
HIV infects CD4+ T-cells, leading to their depletion via direct viral killing, immune-mediated
destruction, and apoptosis. This weakens the immune system, progressing to AIDS (CD4 count <200
cells/µL), where opportunistic infections and cancers emerge.
Pathogenicity:
Highly pathogenic, leading to chronic infection. Untreated, HIV progresses to AIDS in 5–10 years.
Opportunistic infections (e.g., Pneumocystis pneumonia, tuberculosis) and malignancies (e.g.,
Kaposi’s sarcoma) are hallmarks of AIDS.
Symptoms:
Acute phase: Flu-like symptoms (fever, fatigue, rash, lymphadenopathy) 2–4 weeks post-infection.
Chronic phase: Asymptomatic for years, though lymphadenopathy may persist.
AIDS: Weight loss, chronic diarrhea, night sweats, opportunistic infections, neurological symptoms.
Signs:
Lymphadenopathy, oral thrush, skin lesions (e.g., Kaposi’s sarcoma), wasting syndrome, neurological
deficits (e.g., AIDS dementia).
Treatment:
Antiretroviral therapy (ART): Combination of drugs (e.g., nucleoside reverse transcriptase inhibitors,
protease inhibitors, integrase inhibitors) to suppress viral load, restore CD4 counts, and prevent
progression to AIDS.
Prophylaxis: For opportunistic infections (e.g., trimethoprim-sulfamethoxazole for Pneumocystis).
Supportive care: Nutritional support, management of comorbidities.
No cure or vaccine is available, though research continues.
2. Hepatitis Viruses
Causative Agent:
Five major hepatitis viruses:
Hepatitis A virus (HAV)
Hepatitis B virus (HBV)
Hepatitis C virus (HCV)
Hepatitis D virus (HDV; defective, requires HBV co-infection)
Hepatitis E virus (HEV)
History/Origin:
HAV: Recognized since antiquity; identified as a distinct virus in the 1970s.
HBV: Described in 1960s; linked to “serum hepatitis.”
HCV: Identified in 1989 as non-A, non-B hepatitis.
HDV: Discovered in 1977 in HBV patients.
HEV: Identified in 1980s in waterborne outbreaks.
All likely have ancient origins, with zoonotic links (e.g., HEV to pigs).
Classification:
HAV: Picornaviridae, genus Hepatovirus, non-enveloped RNA virus.
HBV: Hepadnaviridae, partially double-stranded DNA virus.
HCV: Flaviviridae, genus Hepacivirus, enveloped RNA virus.
HDV: Unclassified, defective RNA virus (requires HBV).
HEV: Hepeviridae, non-enveloped RNA virus.
Biology:
HAV/HEV: Non-enveloped, stable in the environment, infect hepatocytes, excreted in feces.
HBV: Enveloped, integrates into host DNA, persists in hepatocytes, produces HBsAg (surface
antigen).
HCV: Enveloped, high genetic variability, infects hepatocytes, evades immune response.
HDV: Uses HBV envelope, replicates in hepatocytes, enhances HBV severity.
Mode of Transmission:
HAV/HEV: Fecal-oral (contaminated food/water, poor sanitation).
HBV/HCV/HDV: Bloodborne (needles, transfusions, sexual contact, vertical transmission).
HBV: Also via saliva, semen; highly infectious.
HEV: Zoonotic (undercooked pork, shellfish).
Pathogenesis:
All target hepatocytes, causing inflammation (hepatitis).
HAV/HEV: Acute, self-limiting; rarely chronic.
HBV/HCV: Acute or chronic; chronic infection leads to cirrhosis, hepatocellular carcinoma (HCC).
HDV: Co-infection or superinfection with HBV worsens liver damage.
Pathogenicity:
HAV/HEV: Low; acute illness, full recovery typical.
HBV/HCV: High; 5–10% (HBV) and 50–80% (HCV) progress to chronicity, risking cirrhosis/HCC.
HDV: Very high; accelerates HBV-related liver damage.
Symptoms:
Acute: Fever, fatigue, nausea, jaundice, dark urine, abdominal pain.
Chronic (HBV/HCV): Often asymptomatic until cirrhosis/HCC; fatigue, hepatomegaly.
HEV: Severe in pregnant women (high mortality).
Signs:
Jaundice, hepatomegaly, ascites (in cirrhosis), spider nevi, palmar erythema, encephalopathy
(advanced disease).
Treatment:
HAV/HEV: Supportive care (hydration, rest); HAV vaccine available; HEV vaccine (China only).
HBV: Antivirals (tenofovir, entecavir), interferon; vaccine available.
HCV: Direct-acting antivirals (sofosbuvir, ledipasvir); cure rates >95%; no vaccine.
HDV: Pegylated interferon (limited efficacy); HBV treatment to control co-infection.
Chronic cases: Liver transplant for end-stage disease.
3. Herpesviruses
Causative Agent:
Family Herpesviridae, including:
Herpes simplex virus (HSV-1, HSV-2)
Varicella-zoster virus (VZV)
Epstein-Barr virus (EBV)
Cytomegalovirus (CMV)
Human herpesvirus 6, 7, 8 (HHV-6, HHV-7, HHV-8)
History/Origin:
Herpesviruses are ancient, co-evolving with humans. HSV described in ancient texts; EBV linked to
Burkitt lymphoma in the 1960s; HHV-8 to Kaposi’s sarcoma in the 1990s.
Classification:
Family: Herpesviridae
Subfamilies: Alphaherpesvirinae (HSV-1/2, VZV), Betaherpesvirinae (CMV, HHV-6/7),
Gammaherpesvirinae (EBV, HHV-8).
All are enveloped, double-stranded DNA viruses.
Biology:
Large, enveloped viruses with linear dsDNA. Establish lifelong latency in specific cells (e.g., neurons
for HSV/VZV, B-cells for EBV, monocytes for CMV). Reactivation triggered by stress,
immunosuppression.
Mode of Transmission:
HSV-1: Oral contact, saliva (cold sores).
HSV-2: Sexual contact (genital herpes).
VZV: Respiratory droplets, direct contact (chickenpox/shingles).
EBV: Saliva (kissing, shared utensils; mononucleosis).
CMV: Body fluids (saliva, urine, blood, semen), vertical transmission.
HHV-8: Sexual contact, blood (common in HIV patients).
Pathogenesis:
Infect epithelial cells or lymphocytes, establish latency, and reactivate periodically. Immune evasion
via latency and modulation of host responses. Oncogenic potential (EBV, HHV-8).
Pathogenicity:
HSV: Recurrent mucocutaneous lesions; rare encephalitis.
VZV: Chickenpox (primary), shingles (reactivation).
EBV: Mononucleosis; linked to lymphomas, nasopharyngeal carcinoma.
CMV: Congenital defects, retinitis in immunocompromised.
HHV-8: Kaposi’s sarcoma, primary effusion lymphoma.
Symptoms:
HSV: Painful blisters/sores (oral/genital), fever.
VZV: Rash, fever (chickenpox); unilateral painful rash (shingles).
EBV: Fever, sore throat, fatigue (mononucleosis).
CMV: Asymptomatic or mononucleosis-like; congenital (hearing loss, microcephaly).
HHV-8: Skin l esions (Kaposi’s sarcoma).
Signs:
Vesicular rash (HSV, VZV), lymphadenopathy (EBV), hepatosplenomegaly (CMV, EBV), purple skin
lesions (HHV-8).
Treatment:
HSV: Antivirals (acyclovir, valacyclovir).
VZV: Antivirals (acyclovir for shingles), vaccine (chickenpox, shingles).
EBV: Supportive care; no specific antiviral.
CMV: Ganciclovir, valganciclovir (immunocompromised).
HHV-8: ART for HIV-related cases; chemotherapy for Kaposi’s sarcoma.
No cure; treatment focuses on symptom relief and preventing complications.

Viral Diseases II: Respiratory Viruses,

Arboviruses, Emerging Viral Infections
1. Respiratory Viruses
Causative Agent:
Influenza viruses (A, B, C; Orthomyxoviridae).
Respiratory syncytial virus (RSV; Pneumoviridae).
Rhinoviruses (Picornaviridae).
Coronaviruses (e.g., SARS-CoV-2, MERS-CoV; Coronaviridae).
Parainfluenza viruses (Paramyxoviridae).
History/Origin:
Influenza: Pandemics recorded since 16th century (e.g., 1918 Spanish flu).
RSV: Identified in 1950s.
Rhinoviruses: Common cold known for centuries; viruses identified in 1950s.
Coronaviruses: SARS (2002), MERS (2012), COVID-19 (2019).
Zoonotic origins common (e.g., influenza from birds, SARS-CoV-2 from bats).
Classification:
Influenza: Orthomyxoviridae, enveloped, segmented RNA.
RSV: Pneumoviridae, enveloped RNA.
Rhinoviruses: Picornaviridae, non-enveloped RNA.
Coronaviruses: Coronaviridae, enveloped RNA.
Parainfluenza: Paramyxoviridae, enveloped RNA.
Biology:
Enveloped (except rhinoviruses), single-stranded RNA viruses. Target respiratory epithelium.
Coronaviruses and influenza have spike proteins for cell entry; rhinoviruses use capsid proteins.
Mode of Transmission:
Respiratory droplets (coughing, sneezing).
Aerosols (especially SARS-CoV-2, influenza).
Fomites (rhinoviruses, RSV).
Close contact (RSV, parainfluenza).
Pathogenesis:
Infect respiratory tract (nasopharynx to alveoli), causing epithelial damage, inflammation, and
cytokine release. Severe cases involve systemic spread (influenza) or acute respiratory distress
syndrome (SARS-CoV-2).
Pathogenicity:
Rhinoviruses: Low; mild, self-limiting.
RSV: High in infants/elderly (bronchiolitis, pneumonia).
Influenza: Moderate to high; complications in elderly (pneumonia).
SARS-CoV-2: High; severe pneumonia, multi-organ failure in some.
Symptoms:
Rhinoviruses: Runny nose, sore throat, cough.
RSV: Wheezing, dyspnea, fever (severe in infants).
Influenza: Fever, myalgia, cough, headache.
SARS-CoV-2: Fever, cough, dyspnea, anosmia; severe cases include hypoxia.
Parainfluenza: Croup, bronchiolitis.
Signs:
Fever, nasal congestion, wheezing (RSV), crackles (pneumonia), hypoxia (SARS-CoV-2).
Treatment:
Rhinoviruses: Supportive (decongestants, rest).
RSV: Supportive; palivizumab (monoclonal antibody) for high-risk infants.
Influenza: Antivirals (oseltamivir, zanamivir), vaccines.
SARS-CoV-2: Antivirals (remdesivir, Paxlovid), monoclonal antibodies, corticosteroids; vaccines.
Parainfluenza: Supportive care.
2. Arboviruses
Causative Agent:
Arthropod-borne viruses, including:
Dengue virus (DENV; Flaviviridae).
Zika virus (ZIKV; Flaviviridae).
Chikungunya virus (CHIKV; Togaviridae).
West Nile virus (WNV; Flaviviridae).
Yellow fever virus (YFV; Flaviviridae).
History/Origin:
Dengue: Described in 18th century; global spread with urbanization.
Zika: Identified in 1947 (Uganda); major outbreak in 2015 (Americas).
Chikungunya: Emerged in 1950s (Africa); global spread in 2000s.
WNV: Identified in 1937 (Uganda); U.S. outbreak in 1999.
Yellow fever: Known since 17th century; African origin.
Classification:
DENV, ZIKV, WNV, YFV: Flaviviridae, enveloped RNA.
CHIKV: Togaviridae, enveloped RNA.
Biology:
Enveloped, single-stranded RNA viruses. Replicate in arthropod vectors (mosquitoes, ticks) and
vertebrate hosts. Use surface glycoproteins for cell entry.
Mode of Transmission:
Mosquito bites (Aedes for DENV, ZIKV, CHIKV, YFV; Culex for WNV).
ZIKV: Also sexual, vertical, bloodborne.
YFV: Sylvatic (monkeys) and urban cycles.
Pathogenesis:
Infect skin cells, spread to lymph nodes, and cause viremia. Target various tissues (e.g., endothelium
for DENV, neural tissue for ZIKV/WNV). Severe cases involve hemorrhage (DENV, YFV) or
neurological damage (WNV, ZIKV).
Pathogenicity:
DENV: High in severe dengue (hemorrhagic fever, shock).
ZIKV: High in congenital infections (microcephaly).
CHIKV: Moderate; chronic arthritis.
WNV: High in neuroinvasive disease (encephalitis).
YFV: High; severe liver damage.
Symptoms:
DENV: Fever, rash, joint pain; severe: bleeding, shock.
ZIKV: Mild fever, rash, conjunctivitis; congenital: microcephaly.
CHIKV: Fever, severe joint pain, rash.
WNV: Fever, headache; severe: meningitis, encephalitis.
YFV: Fever, jaundice, bleeding.
Signs:
Rash, petechiae (DENV), conjunctivitis (ZIKV), hepatomegaly (YFV), neurological deficits (WNV).
Treatment:
Supportive care (fluids, pain relief) for all.
YFV: Vaccine available; no specific antiviral.
DENV: Careful fluid management in severe cases.
No vaccines for ZIKV, CHIKV, WNV (except horses for WNV).
3. Emerging Viral Infections
Causative Agent:
SARS-CoV-2 (Coronaviridae).
Ebola virus (Filoviridae).
Nipah virus (Paramyxoviridae).
Lassa virus (Arenaviridae).
Others (e.g., MERS-CoV, avian influenza).
History/Origin:
SARS-CoV-2: Emerged 2019 (Wuhan, China); likely bat origin.
Ebola: First outbreak 1976 (DRC); bat reservoir.
Nipah: Emerged 1998 (Malaysia); bat-to-pig transmission.
Lassa: Identified 1969 (Nigeria); rodent reservoir.
Most have zoonotic origins, driven by deforestation, urbanization.
Classification:
SARS-CoV-2: Coronaviridae, enveloped RNA.
Ebola: Filoviridae, enveloped RNA.
Nipah: Paramyxoviridae, enveloped RNA.
Lassa: Arenaviridae, enveloped RNA.
Biology:
Enveloped RNA viruses with high mutation rates (except Lassa). Target various cells (e.g., endothelial
for Ebola, neuronal for Nipah, respiratory for SARS-CoV-2).
Mode of Transmission:
SARS-CoV-2: Respiratory droplets, aerosols.
Ebola: Direct contact with body fluids, fomites.
Nipah: Contact with infected pigs, bats, or humans; foodborne (date palm sap).
Lassa: Contact with rodent excreta, human body fluids.
Pathogenesis:
Cause systemic infection with immune dysregulation. Ebola/Lassa cause hemorrhagic fever; SARS-
CoV-2 leads to respiratory failure; Nipah causes encephalitis.
Pathogenicity:
SARS-CoV-2: High in severe cases (ARDS).
Ebola: Very high (50–90% mortality).
Nipah: High (40–75% mortality).
Lassa: Moderate (15–20% in hospitalized cases).
Symptoms:
SARS-CoV-2: Fever, cough, dyspnea, anosmia.
Ebola: Fever, bleeding, diarrhea, multi-organ failure.
Nipah: Fever, encephalitis, coma.
Lassa: Fever, sore throat, bleeding, deafness.
Signs:
Hypoxia (SARS-CoV-2), petechiae (Ebola, Lassa), neurological deficits (Nipah), hepatomegaly
(Lassa).
Treatment:
SARS-CoV-2: Antivirals (Paxlovid), corticosteroids, vaccines.
Ebola: Supportive care, monoclonal antibodies (e.g., REGN-EB3); vaccine (rVSV-ZEBOV).
Nipah: Supportive care; ribavirin (limited efficacy).
Lassa: Ribavirin, supportive care.
Public health measures (quarantine, contact tracing) critical.
Summary:
HIV: Chronic, immunosuppressive, bloodborne/sexual; treated with ART.
Hepatitis viruses: Liver-targeting; HAV/HEV fecal-oral, HBV/HCV/HDV bloodborne;
antivirals/vaccines available for some.
Herpesviruses: Latent, diverse diseases (sores to cancers); antivirals for management.
Respiratory viruses: Droplet/aerosol spread; range from mild (rhinoviruses) to severe (SARS-CoV-2);
vaccines for some.
Arboviruses: Mosquito-borne; cause fever, hemorrhage, neurological disease; supportive care, YFV
vaccine.
Emerging viruses: Zoonotic, high mortality (Ebola, Nipah); limited treatments, vaccines for some.
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