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HIV-1, human immunodeficiency virus type 1, is a human retrovirus in the genus Lentivirus and family Retroviridae. It can cause acquired immunodeficiency syndrome, an advanced stage of HIV infection; the virus and the disease stage are distinct concepts.^[ref]

Its virion has a viral envelope and an internal core containing the RNA genome and replication machinery. During infection, reverse transcription produces a DNA copy, which becomes integrated into host-cell DNA as a provirus. This RNA-to-DNA step is a defining part of retroviral replication.^[ref] The primate lentiviruses use CD4 together with a chemokine receptor for cell recognition and entry.^[ref]

An idealized counting example distinguishes molecular and particle quantities. An orthoretroviral particle packages a dimer of genomic RNA: a preparation containing 100 intact such particles would contain 200 packaged RNA molecules. Counting RNA molecules therefore need not give the same number as counting virions.^[ref]

Actual nucleic-acid measurements can also detect material outside complete particles. Particle assembly, integration and successful infection require different evidence, so the measured object must be specified rather than treating every virus-associated signal as the same biological quantity.

Human immunodeficiency virus is the name used for two related retroviruses, HIV-1 and HIV-2, whose infection can lead to AIDS. The virus and the disease stage are distinct: AIDS is the most advanced stage of human immunodeficiency virus infection, rather than the name of every infection.^[ref]

Both belong to Lentivirus, within Orthoretrovirinae and Retroviridae. Their replication connects an RNA genome, a DNA intermediate formed by reverse transcription, and an integrated provirus. In primate lentiviruses, entry involves CD4 and a chemokine receptor; identifying a cell receptor and measuring subsequent virus production are distinct experimental questions.^[ref][ref]

A constructed measurement example distinguishes a molecular quantity from a biological outcome. Suppose an assay reports 100 viral RNA copies in an analysed equivalent of one microlitre of plasma. The corresponding viral load is $100\times 1000=100,000$ RNA copies per millilitre, assuming the assay's stated calibration and volume correction. That count is not a direct count of infectious virions, and it does not by itself specify a person's disease stage. The measured material, normalization and biological question must all be stated.

Orthoretrovirinae is the subfamily of Retroviridae containing Lentivirus and several other retroviral genera. It includes human immunodeficiency virus and feline immunodeficiency virus. The family placement describes a replication strategy; it does not imply one host range or one disease outcome for all members.^[ref]

A typical virion packages two copies of its RNA genome. After entry and release of the viral core into a host cell, reverse transcription produces DNA that can become an integrated provirus. Proteolytic processing of a viral polyprotein also releases functional components during maturation.^[ref][ref]

An invented counting example clarifies the two-copy description. If each packaged RNA molecule has 10,000 nucleotides, the pair contains 20,000 RNA nucleotides in total. The length of one genome copy is still 10,000 nucleotides. A corresponding 10,000-base-pair double-stranded DNA molecule contains 20,000 DNA nucleotides, but its length is conventionally reported in base pairs. Copy count, nucleotide count and base-pair length answer different questions.

The subfamily's genera are distinguished in part by phylogenetic analysis of conserved reverse-transcriptase regions. A shared enzyme mechanism can coexist with differences in accessory proteins, host distribution and cellular targets. Observing the shared mechanism therefore provides a classification clue while leaving those other biological properties to be determined.^[ref]

Retrovirus studies showed that a transmissible agent can cause a tumour and, more unexpectedly, that a viral transforming gene can derive from an ordinary cellular gene. This connected infectious cancer models to the molecular control of normal cell growth.

Peyton Rous transmitted a chicken sarcoma using material from a tumour and showed that a cell-free filtrate could transmit the disease. The agent could therefore be separated from intact tumour cells, arguing against simple transplantation of the malignant cells as the explanation.^[ref] This established a filterable tumour-causing agent, not yet its RNA genome, replication mechanism or a claim that every cancer is infectious. In repeating such an experiment, an uninoculated or sham-treated group and a preparation verified to lack viable donor cells would be essential comparators; host susceptibility and the preparation's retained infectivity would also matter.

The later Rous sarcoma virus system made transformation experimentally tractable. Infected cultured fibroblasts can lose contact inhibition, change morphology and form foci against a background of untransformed cells. Such assays distinguish efficient transformation from the slower and more complex endpoint of tumour formation in an animal. Temperature-sensitive transforming mutants allow the phenotype to be switched by changing conditions, while transformation-defective viruses can still replicate. This separates a transforming function from the basic machinery required to produce virus.

The retroviral life cycle explains persistent genetic change. Viral RNA is copied into DNA by reverse transcriptase; the resulting DNA can integrate into the cellular genome as a provirus. Demonstration of RNA-dependent DNA synthesis in Rous-virus particles gave biochemical support to this route of information transfer.^[ref] Template dependence, nuclease sensitivity and controls for contaminating cellular enzymes are needed to infer an RNA-templated polymerase rather than merely observe incorporation of labelled nucleotides. Integration then allows stable expression of viral genes through ordinary cellular transcription.

Comparison of transforming and transformation-defective viral genomes identified v-src as a transforming determinant. A crucial next question was whether src-like sequence existed only in tumour viruses. A probe enriched for transformation-specific viral sequences hybridized to DNA from normal birds, including multiple avian species. This showed that related information was present in normal cellular genomes, with evolutionary conservation rather than only virus-associated occurrence.^[ref] The cellular counterpart, c-src, is a proto-oncogene: a normally regulated cellular gene that can become oncogenic when its expression or activity is altered. Viral capture and modification of cellular growth-control information therefore explain why a virus can carry a potent growth-deregulating gene.

The Src product linked genotype to a biochemical mechanism. Its kinase activity was shown to phosphorylate tyrosine residues, establishing an unusual regulatory chemistry at the time and connecting transformation to deregulated protein phosphorylation.^[ref] The viral product has altered regulation compared with normal cellular Src, so persistent signalling can disrupt growth, adhesion and cytoskeletal control. The lesson is not that a normally expressed proto-oncogene is inherently malignant: context, dosage and regulatory state matter. Immunoprecipitate kinase assays need controls because an associated kinase could otherwise be mistaken for the precipitated protein's catalytic activity; biochemical and genetic tests strengthen the attribution.

Other retroviruses supplied a second route. Slowly transforming avian leukosis viruses need not carry a captured oncogene; integration near a cellular gene can alter its expression through viral regulatory sequences. Promoter-insertion studies of the MYC proto-oncogene demonstrated this principle.^[ref] Recurrent integrations near the same gene across independent tumours provide more persuasive evidence than one integration in one tumour, and expression and functional tests help distinguish a driver event from an incidental integration.

Together these experiments established separable mechanisms of viral oncogene acquisition and insertional oncogenesis, revealed cellular proto-oncogenes and identified deregulated signalling as a cause of transformation. They do not imply that retroviral integration explains every tumour, or that a transformed culture has all the properties of an invasive cancer. Their wider importance is that normal growth-regulatory genes, when altered, can drive malignant behaviour even outside the original infectious setting.

A provirus is a viral DNA form integrated into a cellular genome. Its location and regulatory sequences can influence both viral expression and neighbouring cellular genes.

The retroviral life cycle includes entry, RNA-to-DNA copying by reverse transcriptase, a DNA intermediate and gene expression followed by particle production. Integration as a provirus can make the genetic change persistent across cell divisions.

Retroviridae is a taxonomic family of enveloped viruses whose replication involves reverse transcription and integration of the resulting DNA into host-cell DNA. The integrated form is a provirus, from which host machinery can make viral RNA. Thus the replication cycle links RNA and DNA forms rather than remaining entirely in one nucleic-acid form.^[ref]

A virion contains a viral envelope, an internal core, genomic nucleic acid and replication enzymes. Orthoretrovirinae package a dimer of single-stranded RNA. In Spumaretrovirinae, reverse transcription can already be partly completed in the particle, so a family-wide description should not require every virion to contain only RNA.^[ref]

HIV-1, in the genus Lentivirus, is one member of this broader family. The family name therefore supplies a classification shared by multiple genera, rather than another name for HIV-1 alone.

The RNA-to-DNA-to-RNA cycle also clarifies measurement. A test detecting a proviral DNA sequence addresses a different molecular form from a test detecting packaged RNA. Demonstrating one intermediate can support the proposed replication pathway, but its abundance alone does not count every completed infectious particle. The assay must identify which stage and material it measures.