Viruses are not considered living organisms because they are obligate intracellular parasites, meaning they must infect a host cell to replicate. They are ultra-microscopic, ranging from 20 to 450 nanometers, and are much smaller than bacteria. Viruses are not cellular, have a compact structure, and possess few or no enzymes, relying on host cell machinery for replication. Their core contains either DNA or RNA, but generally not both, and this nucleic acid can be single-stranded, double-stranded, circular, or linear. Viral surfaces have molecules for specific attachment to host cells, allowing them to hijack the host's machinery. The size of a virus does not correlate with its pathogenicity.

A virion, a fully formed infectious virus, consists of a protein shell or capsid and a nucleic acid core. All viruses have a capsid, a protein coat that protects the nucleic acids. Some viruses also have an envelope, a phospholipid membrane derived from the host cell, making them enveloped viruses. Viruses without this envelope are called naked viruses. Enveloped viruses are more sensitive to antimicrobial chemicals because their lipid membrane can be dissolved. The central core contains the viral genome (DNA or RNA), which carries genes for invading host cells and redirecting cellular activity for viral production. Some viruses also have matrix proteins and a few enzymes.

The capsid, made of repeating protein subunits called capsomeres, encloses and protects the nucleic acids. The envelope, present in some viruses (mainly animal viruses), surrounds the capsid and helps the virus hide from the host's immune system by mimicking host cell antigens. Envelopes contain carbohydrate-protein complexes called spikes, crucial for attachment to host cells and determining cell specificity. Enveloped viruses can be pleomorphic (many shapes) due to the fluid nature of their membrane. Both the capsid and envelope protect the virion outside the host and facilitate binding and penetration of viral genetic material into suitable host cells.

Viruses generally lack enzymes for their own metabolism, such as protein synthesis or ATP generation. However, some viruses possess specific enzymes. Polymerases are used to synthesize new DNA or RNA. Replicases are specific for copying RNA from an RNA template. Reverse transcriptase, found in retroviruses like HIV, synthesizes DNA from an RNA template, which is a key target for antiviral drugs. Lysozyme, found in bacteriophages, degrades bacterial cell walls to facilitate DNA injection into the host cell.

Viral capsids exhibit four main morphologies: helical, polyhedral, complex, and enveloped. Helical viruses have a hollow cylinder with nucleic acids inside, such as Ebola and rabies. Polyhedral viruses are many-sided, typically 20-sided (icosahedron), like adenoviruses. Complex viruses, such as bacteriophages, combine helical and polyhedral structures. Enveloped viruses, like influenza, are roughly spherical but pleomorphic due to their fluid envelope. The capsid inside an enveloped virus can be either helical or polyhedral.

The animal virus multiplication cycle involves six stages: adsorption (attachment), penetration, uncoating, synthesis, assembly, and release. Adsorption involves the virus binding to specific host cell receptors, determining its host range (narrow for Hepatitis B, broad for rabies). Penetration is when the virus enters the cell, typically via receptor-mediated endocytosis or fusion. Uncoating is the release of the viral nucleic acid from its capsid. Synthesis involves the production of viral components. Assembly is the construction of new virions. Release can occur through budding (exocytosis), where the virus acquires an envelope from the host membrane without immediately destroying the cell, or through cell lysis, which ruptures and kills the host cell.

Viruses, being obligate intracellular parasites, require living cells for cultivation. Methods include infecting living animals, embryonated eggs, or using cell cultures. In cell cultures, viral infection can be detected by cytopathic effects (CPE), such as changes in cell size/shape, inclusion bodies, cell fusion, lysis, or DNA alteration, and transformation into cancer cells. Identification primarily uses serological tests (e.g., Western blot for antibodies or viral proteins) and nucleic acid-based methods (e.g., RFLP, PCR for specific viral sequences). Treatments include entry inhibitors (e.g., Tamiflu), nucleic acid synthesis inhibitors (e.g., Acyclovir for herpes, AZT for HIV), and assembly/release inhibitors (e.g., protease inhibitors, Tamiflu affecting budding). Interferons, naturellement produced by infected cells, can be used to magnify the immune response and prevent viral spread.

Viral infections can be acute, latent, or persistent. Acute infections have a rapid onset, brief symptoms, and quick resolution, with early production of virions eliminated by the immune system. Latent infections involve the virus remaining asymptomatic within cells, potentially reactivating due to stimuli (e.g., herpes simplex virus causing cold sores, varicella zoster virus causing shingles). Persistent infections involve continuous, slow production of virions over a long period, which can be fatal (e.g., measles virus, HPV leading to cervical cancer). Some animal viruses are oncogenic (oncoviruses), permanently altering host cell genetic material, leading to uncontrolled growth and potentially cancer (e.g., HPV, Epstein-Barr virus, Hepatitis virus).

Bacteriophages (phages) infect bacteria. Their multiplication cycle is similar to animal viruses but with key differences. Phage attachment occurs via tail fibers binding to the bacterial cell wall. Entry involves the phage injecting its DNA into the host cell via lysosyme action, which degrades the cell wall. Uncoating is not necessary as the capsid remains outside. Biosynthesis and maturation occur in the cytoplasm, producing and assembling new phage particles. Release happens only by lysis, as bacteria have cell walls preventing budding, and phages lack envelopes. Phage plaques on bacterial lawns indicate regions of lysis. Some phages undergo a lysogenic cycle, where viral DNA integrates into the host chromosome (prophage) and replicates with the host genome without actively producing new virions. This can lead to phage conversion, giving the bacterium new properties, such as toxin production (e.g., E. coli O157:H7 producing Shiga toxin).

Prions are proteinaceous infectious particles, misfolded proteins with no nucleic acids, highly resistant to sterilization. They cause transmissible spongiform encephalopathies, fatal neurodegenerative diseases in animals (e.g., scrapie in sheep, mad cow disease in cattle) and humans (e.g., Creutzfeldt-Jakob syndrome). Mad cow disease transmission to humans occurred through the consumption of undercooked beef from infected cattle. Other non-cellular infectious agents include satellite viruses, which depend on other viruses for replication (e.g., adeno-associated virus requiring adenovirus, Delta agent requiring Hepatitis B virus). Viroids are short pieces of RNA with no protein coat, currently only identified in plants.