Microbial and Fungal Diversity

This is Unit Nine of Biology, Part One: viruses. A virion is a genome inside a protein coat, sometimes wrapped in a lipid envelope — and that envelope is taken from a host cell rather than made. It has no ribosomes, no organelles, and no metabolism of its own. Which cells it can infect is set by receptors. A virus attaches only where a matching surface molecule exists, and that molecule is a normal host-cell component the virus exploits. The cell did not evolve it to admit viruses. Classification here works differently from the rest of biology. Baltimore grouping sorts viruses by how each genome type gets converted into messenger R N A, not by shape or host — so two viruses with the same kind of genome can land in different groups if their route to messenger R N A differs. Then two questions the field has not settled: where viruses came from, and whether they are alive at all. The course gives both sides of the second and notes that both accept the same facts about a virion — they differ on which facts should count as defining life. By the end you will be able to do five things. One: say what a virion is. Two: say what Baltimore sorts by. Three: say why the life question is open. Four: tell lytic from lysogenic. Five: say why combination therapy works.

Four entries building the particle. Structure, shape, what decides its host range, and a genome that comes in more varieties than any cell's. Each entry narrows what a virion can be assumed to have.

The particle.

Bio 1901 Virion Structure: Genome, Capsid, and Envelope

A virion holds a nucleic acid genome inside a protein capsid, sometimes wrapped in a lipid envelope taken from a host cell — influenza is enveloped, poliovirus is not. A virion carries no ribosomes and no organelles of its own, and any envelope it has is borrowed rather than built.

Four shapes.

Bio 1903 Four Capsid Shape Classes

Viral capsids fall into four shape classes — helical, icosahedral, enveloped, and head-and-tail — built from repeating protein subunits, so tobacco mosaic virus is helical and a bacteriophage combines an icosahedral head with a helical tail. Shape alone predicts neither a virus's disease nor its host; it helps sort families.

Who it can infect.

Bio 1905 Viral Receptors and Host Specificity

A virus attaches only to host cells bearing a matching surface receptor, which sets which species and cell types it can infect at all — a cell lacking the right receptor cannot be infected by that route. The receptor is a normal host-cell molecule the virus exploits; the cell did not evolve it to admit viruses.

Any nucleic acid.

Bio 1907 Viral Genome Types: DNA and RNA

Unlike cellular life, which always uses D N A, a viral genome may be D N A or R N A, single- or double-stranded, linear or circular — herpesviruses carry double-stranded D N A, influenza a segmented single-stranded R N A. Genome type must be determined rather than presumed from how cells work.

Three entries on a classification scheme built on a single question: how does this genome become messenger R N A? That question cuts across shape and host entirely, which is what makes the scheme useful.

The logic.

Bio 1909 The Baltimore Classification Logic

Baltimore classification sorts viruses by how each genome type is converted into messenger R N A during replication, rather than by shape or host — a double-stranded D N A virus transcribes directly, while a single-stranded R N A virus first needs an enzyme to build a complementary strand. Two viruses sharing a genome type can land in different groups if their route differs.

The first three.

Bio 1911 Baltimore Groups I–III

Group one carries double-stranded D N A, group two single-stranded D N A, and group three double-stranded R N A, each converted to messenger R N A differently — herpesviruses transcribe much as a host cell does, rotavirus transcribes from double-stranded R N A. Group two's genome must first become double-stranded; it cannot be transcribed single-stranded.

The rest.

Bio 1913 Baltimore Groups IV–VII and Retroviruses

Groups four and five carry single-stranded R N A read or copied into messenger R N A; groups six and seven use reverse transcriptase to make D N A from R N A — H I V, a group six retrovirus, reverse-transcribes its genome before inserting it into the host's. Reverse transcription runs counter to a cell's usual direction; retroviruses are the named exception.

Three entries, and none of them resolves. Where viruses came from has three competing hypotheses. Whether a virus is alive gets two entries — one stating the case against, one stating the case for — and the second is careful about what actually separates the two positions.

Three origins.

Bio 1915 Three Hypotheses for Viral Origin

Three hypotheses compete for how viruses originated — regressive, progressive and virus-first — and the field has not settled which, if any, is correct. The regressive hypothesis proposes viruses devolved from free-living cells; it does not claim viruses are ancestors of cells but the reverse.

The case against.

Bio 1917 "A Virus Is a Living Organism"

Calling a virus a living organism overstates an unsettled question, since by the cellular-life criteria most courses teach, a virus fails several tests — a virion has no metabolism, makes no energy of its own, and cannot reproduce without hijacking host machinery. This states one basis for denying viral life; the next entry gives the basis for granting it.

The case for.

Bio 1919 Whether a Virus Is Alive, Revisited

Whether a virus is alive is genuinely open: a virion has no metabolism of its own, yet its genome evolves and adapts inside a host. Both sides accept the same facts about a virion — they differ only in which of those facts should count as defining life.

Three entries. Six steps that must run in order, then two strategies — one that destroys the host to get out, and one that integrates and waits, sometimes for years.

Six steps.

Bio 1921 Steps of Viral Replication, Overview

Most viral infections proceed through six steps in order — attachment, entry, uncoating, replication, assembly and release — as when a bacteriophage attaches, injects its genome, replicates, assembles and lyses the cell. Skipping a step, such as failing to uncoat the genome, halts the cycle; a virus cannot replicate past a blocked step.

Bursting out.

Bio 1923 The Lytic Cycle

In the lytic cycle a virus replicates inside its host, assembles new virions, and bursts the cell open to release them — a bacteriophage lysing a bacterium and releasing many particles at once. Lysis kills the host cell, so a virus using only this cycle cannot leave without destroying its host.

Waiting.

Bio 1925 The Lysogenic Cycle and Latency

In the lysogenic cycle a temperate virus's genome integrates into the host as a prophage, replicating along with it until a stressor triggers the lytic cycle — lambda phage integrating into a bacterial chromosome, herpesviruses persisting latently in nerve tissue for years. A prophage is not cleared; it can excise and re-enter the lytic cycle long afterward.

Two entries on entry and exit, one for plants and one for animals. A plant virus has no active way in at all, and an animal virus has two ways out with different consequences for the cell.

Needing a wound.

Bio 1927 Plant Virus Transmission

To enter a new host plant, a plant virus needs mechanical damage such as an insect bite, since it has no active entry mechanism — aphids feeding on sap carry viruses between plants. A plant virus can also pass vertically from parent to offspring, so infection does not always come from an outside vector.

Two exits.

Bio 1929 Animal Virus Entry and Exit

Animal viruses enter cells by endocytosis or membrane fusion, then exit either by budding, which spares the cell, or by lysis, which kills it — influenza buds without killing, while non-enveloped rhinoviruses accumulate until the cell lyses. Budding does not mean the cell is undamaged; function can be impaired while the cell survives.

Four entries, and this is where the lecture's medical disclaimer earns its place. What some viruses do to cell-cycle control, and three things medicine does in response — each stated as mechanism with its own limit.

Cancer risk.

Bio 1931 Oncogenic Viruses

An oncogenic virus can cause cancer by introducing genes that drive unregulated cell growth or by disrupting genes that normally restrain it — human papillomavirus is associated with cervical cancer, hepatitis C with liver cancer after chronic infection. Most viral infections are not oncogenic; only those interfering with cell-cycle regulation carry this risk.

Training immunity.

Bio 1933 Vaccines: Mechanism of Protection

A vaccine builds immunity by exposing the immune system to a live-attenuated, killed or subunit form of a virus without causing full disease — a killed-virus vaccine cannot cause infection, a live-attenuated one replicates poorly. The live-attenuated form carries a small risk of reverting to a disease-causing form that the killed form does not.

Blocking a protein.

Bio 1935 Antiviral Drug Mechanism

An antiviral drug blocks a viral protein's function without targeting proteins the host cell's healthy metabolism depends on — one influenza drug inhibits an enzyme new virions need to detach and spread. That specificity to viral-only proteins is what limits side effects; a drug hitting host proteins would harm the patient.

Several at once.

Bio 1937 Combination Therapy Against a Fast-Mutating Virus

Combining antiviral drugs that target different replication steps makes resistance to all of them far less likely — H I V therapy mixes drugs from two or three classes for exactly that reason. A single drug alone lets a fast-mutating R N A virus evolve resistance quickly; combination therapy slows that evolution.

Two entries. One covers agents that fit no definition on offer — a protein with no genome, and a genome with no protein — and then the capstone runs one infection from attachment to clearance.

Less than a virus.

Bio 1938 Subviral Agents: Prions and Viroids

A subviral agent infects without a standard virion: a prion is protein alone, templating a normal protein into its own misfolded shape, and a viroid is a short circular R N A with no protein coat, copied by the host's own enzymes. They are mirror images of each other, and neither fits the definition of a virus.

The capstone. One infection.

Bio 1939 Tracing a Viral Infection from Attachment Through Immune Clearance and Treatment

An enveloped R N A virus meets a respiratory tract. Surface glycoproteins bind a matching receptor, which is what fixes host and tissue. The virion enters by endocytosis or fusion, the six-step cycle redirects the cell's machinery, and new virions bud out — spreading without immediately killing the cell. This virus is not oncogenic, so no elevated cancer risk attaches. Prior vaccination would have the immune system recognise the surface proteins at once; without it, an antiviral can slow spread. Each stage depends on the one before, so treatment aimed at the wrong stage does not stop infection.

Five things to carry out of Part One. A virion is a nucleic acid genome inside a protein capsid, sometimes wrapped in a lipid envelope taken from a host cell. It has no ribosomes, no organelles and no metabolism. Which cells it can infect is set by matching a receptor — a normal host molecule the virus exploits rather than one the cell evolved to admit it. Baltimore classification sorts viruses by how each genome type becomes messenger R N A during replication, not by shape or host. That is why two viruses with the same kind of genome can sit in different groups, and why the retroviruses — which make D N A from R N A — are the named exception to a cell's usual direction. Whether a virus is alive is genuinely open, and both sides accept the same facts. A virion has no metabolism and cannot reproduce without a host, which is the case against. Its genome evolves and adapts inside that host, which is the case for. The disagreement is about which facts should count as defining life. The lytic cycle replicates, assembles and bursts the cell open, so a virus using it alone cannot leave without killing its host. The lysogenic cycle integrates the viral genome into the host as a prophage, replicating quietly with it until a stressor triggers lysis — which is why a prophage is not cleared. And combination therapy slows resistance because it targets several replication steps at once. A fast-mutating R N A virus can evolve resistance to one drug quickly; evolving resistance to two or three at the same time is far less likely. Part Two turns to prokaryotes — bacteria and archaea, their structure, their metabolism, and what they do for and to us.