Viruses: Structure, Classification, and Replication

What is a Virus? Differences Between Viruses and Bacteria

• Viruses are acellular infectious agents, typically 20–1000 nm in size, composed of a single type of nucleic acid (DNA or RNA) surrounded by a protein coat (capsid), and sometimes a lipid envelope.

• Living Status: Viruses are not considered living outside a host cell; they are inert until they infect a host, where they become metabolically active and replicate.

• Reproduction: Viruses require a living host cell for replication, utilizing the host's cellular machinery.

• Metabolism: Viruses lack metabolic enzymes and cannot generate ATP independently.

• Bacteria are larger, have both DNA and RNA, possess a plasma membrane and ribosomes, and can reproduce independently via binary fission.

Key Differences Table:

Classification of Viruses

• Baltimore Classification System: Categorizes viruses into seven groups based on nucleic acid type and replication strategy (e.g., Group VI: retroviruses; Group VII: DNA viruses using reverse transcriptase).

• Viral Taxonomy: The International Committee on Taxonomy of Viruses (ICTV) classifies viruses into orders, families (ending in -viridae), genera (-virus), and species.

• Viral Species: Defined by shared characteristics such as morphology, genes, enzymes, and ecological niche.

Purification and Cultivation of Viruses in the Laboratory

• Cell Culture: Viruses are grown in continuous cell lines (e.g., HeLa cells) for isolation and study. Cultures must be monitored to prevent contamination.

• Bacteriophage Cultivation: Bacteriophages are grown using the plaque method, where clear zones (plaques) on bacterial lawns indicate viral presence.

• Viral Identification: Methods include serological assays (e.g., ELISA), observation of cytopathic effects, and PCR-based techniques.

Replication: Bacteriophage vs. Animal Virus

RNA Viruses vs. DNA Viruses

• Genetic Material: RNA viruses have RNA; DNA viruses have DNA.

• Replication Site: RNA viruses usually replicate in the cytoplasm; DNA viruses often in the nucleus.

• Enzymes: RNA viruses use RNA-dependent RNA polymerase (not found in host cells).

• Mutation Rate: RNA viruses mutate more rapidly due to lack of proofreading.

• Example: SARS-CoV-2 is a single-stranded RNA virus.

Antigenic Shift in Influenza Viruses

• Influenza A viruses have a segmented RNA genome (8 segments), allowing for antigenic shift—a major genetic reassortment when two strains infect the same cell.

• This can create new combinations of surface antigens (hemagglutinin and neuraminidase), leading to pandemics.

• Mixing often occurs in pigs, which can be infected by both human and avian influenza viruses.

Viruses and Cancer (Oncogenesis)

• Some viruses cause cancer by integrating into host DNA, causing chromosomal breakage, or activating oncogenes.

• Transformed cells lose contact inhibition and grow uncontrollably.

• Examples: Retroviruses (HTLV-1, HTLV-2), DNA viruses (e.g., HPV, hepatitis B).

Bacteriophage Life Cycles

• Lytic Cycle: Phage attaches, injects DNA, replicates, assembles, and lyses host cell to release new phages.

• Lysogenic Cycle: Phage DNA integrates into host genome (prophage), replicates with host, can later enter lytic cycle.

• Animal viruses may also have latent or chronic cycles, sometimes integrating into host DNA (e.g., retroviruses).

Prions

• Prions are infectious proteins (no nucleic acid) that cause neurodegenerative diseases by inducing misfolding of normal proteins (PrPC to PrPSc).

• Misfolded proteins aggregate, damaging brain tissue (e.g., Creutzfeldt-Jakob disease).

Principles of Disease and Epidemiology

Etiology vs. Pathogenesis

• Etiology: Study of the cause or origin of a disease (e.g., Mycobacterium tuberculosis causes tuberculosis).

• Pathogenesis: Study of the development and progression of disease after the cause is established.

Types of Human Microbiota

• Normal Microbiota: Permanent residents, usually non-pathogenic (e.g., Escherichia coli in intestines).

• Transient Microbiota: Temporary residents, present for days to months.

• Microbial Diversity by Region: Skin (low moisture), eyes (protected by tears), nose/throat (mucus), mouth (nutrient-rich), large intestine (most abundant), urinary/genital systems (pH-influenced).

Types of Symbiotic Relationships

• Commensalism: One benefits, other unaffected (e.g., Staphylococcus epidermidis on skin).

• Mutualism: Both benefit (e.g., E. coli in intestine).

• Parasitism: One benefits at other's expense (e.g., influenza virus in humans).

Sepsis

• Sepsis: Systemic inflammatory response to infection, may progress to severe sepsis (organ dysfunction) and septic shock (low blood pressure).

• Signs: Fever, chills, rapid breathing/heart rate. High mortality if untreated.

Signs vs. Symptoms

• Signs: Objective, measurable (e.g., fever, rash).

• Symptoms: Subjective, felt by patient (e.g., pain, fatigue).

• Example (Sepsis): Signs—fever, lymphangitis; Symptoms—chills, rapid breathing.

Endemic, Epidemic, Pandemic

• Endemic: Constantly present in a population (e.g., common cold).

• Epidemic: Sudden increase in cases in a region (e.g., seasonal influenza).

• Pandemic: Global epidemic (e.g., COVID-19).

Types of Bacterial Infections

• Local: Confined to small area (e.g., abscess).

• Systemic: Spread throughout body (e.g., measles).

• Focal: Local origin, spreads to other sites.

• Sepsis/Septicemia: Microbes/toxins in blood.

• Bacteremia/Toxemia: Bacteria/toxins in blood.

• Primary/Secondary: Initial vs. subsequent infection.

• Asymptomatic: No symptoms, but pathogen present.

Herd Immunity

• Occurs when enough individuals are immune (via vaccination or infection) to prevent disease spread.

• Protects vulnerable populations (e.g., infants, immunocompromised).

Predisposing Factors

• Nutrition: Malnutrition increases risk.

• Sex: Some infections more common in one sex.

• Genetics: Inherited disorders affect susceptibility.

• Climate: Seasonal changes affect transmission.

• Age: Young and elderly more susceptible.

Stages of Disease

1. Incubation Period: Time between infection and symptoms.

2. Prodromal Period: Mild symptoms appear.

3. Period of Illness: Most severe symptoms.

4. Period of Decline: Symptoms subside.

5. Period of Convalescence: Recovery and return to normal.

Reservoirs of Infection

• Human: Symptomatic or asymptomatic carriers.

• Animal: Zoonoses (e.g., rabies, Lyme disease).

• Nonliving: Soil, water (e.g., Legionella in water systems).

Vectors and Transmission

• Vectors: Organisms (often arthropods) that transmit pathogens.

• Mechanical Transmission: Passive transfer (e.g., flies carrying pathogens on feet).

• Biological Transmission: Pathogen reproduces in vector (e.g., mosquito transmits malaria).

Types of Disease Transmission

• Contact: Direct (person-to-person), indirect (fomites), droplet (cough/sneeze).

• Vehicle: Airborne, waterborne, foodborne.

• Vector: Mechanical or biological.

Healthcare-Associated Infections (HAIs)

• Sources: Hospital environment, compromised hosts, chain of transmission.

• Prevention: Sterilization, infection control, antimicrobial stewardship.

Microbial Mechanisms of Pathogenicity

Skin as a Barrier and Microbial Entry

• Physical Barrier: Keratinized, tightly packed cells resist invasion.

• Dryness and Acidic Secretions: Inhibit microbial growth.

• Entry Points: Breaks in skin, hair follicles, sweat ducts, parenteral route (punctures/injections).

ID50 and LD50

• ID50 (Infectious Dose 50): Number of microbes needed to infect 50% of a population.

• LD50 (Lethal Dose 50): Amount of toxin required to kill 50% of a population.

Formula (generalized):

Adhesins and Ligands

• Adhesins/Ligands: Surface molecules on pathogens that bind to host cell receptors, facilitating attachment.

• Examples: Streptococcus mutans (glycocalyx), E. coli (fimbriae), Neisseria gonorrhoeae (fimbriae), influenza virus (HA spike).

Bacterial Evasion of Host Immunity

• Capsules: Prevent phagocytosis (e.g., Streptococcus pneumoniae).

• Cell Wall Components: M protein, mycolic acid resist immune attack.

• Enzymes: Kinases, hyaluronidase, collagenase aid spread.

• Antigenic Variation: Surface antigen changes evade antibodies.

• Biofilms: EPS matrix protects from phagocytes.

Direct Damage by Bacteria

• Utilize host nutrients, produce waste, cause cell rupture.

• Induce host cell engulfment, penetrate cells, or produce toxins.

Endotoxins vs. Exotoxins

Cytopathic Effects of Viruses

• Cytocidal: Cell death.

• Noncytocidal: Cell damage without death.

• Disruption of cell junctions, cytokine storm, inhibition of synthesis, lysosomal enzyme release, chromosomal changes.

Pathogenicity of Protozoa and Parasites

• Cyst Formation: Survival outside host.

• Cell Invasion: Intracellular reproduction (e.g., Plasmodium).

• Attachment: Specialized structures (e.g., Giardia).

• Antigenic Variation: Frequent surface antigen changes (e.g., Trypanosoma).

Additional info: Where details were brief or implied, academic context was added for clarity and completeness, such as expanded definitions, examples, and tables for comparison.