lever its way into cells. The individual viral unit, one particle, standing intact outside a cell, is called a virion. The capsid also defines the exterior shape of a virus. Virions of Ebola and Marburg, for instance, are long filaments, which is why they’ve been placed in a group known as filoviruses. Other viruses have particles that are spherical, or ovoid, or helical, or icosahedral (twenty-sided, like a soccer ball designed by Buckminster Fuller). HIV-1 particles are globular. Rabies virions are shaped like bullets. A plate of Ebola virions mixed with Hendra virions would resemble capellini in a light sauce of capers.
Many viruses are wrapped with an additional layer, known as an envelope, comprising not only protein but also lipid molecules drawn from the host cell—in some cases, pulled from the wall of the cell when the virion made its exit. Across the outer surface of the envelope, the virion may be festooned with a large number of spiky molecular protuberances, like the detonator stubs on an old-fashioned naval mine. Those spikes serve a crucial function. They’re specific to each kind of virus, with a keylike structure that fits molecular locks on the outer surface of a target cell; they allow the virion to attach itself, docking like one spaceship to another, and they open the way in. The specificity of the spikes not only constrains which kinds of host a given virus can infect but also which sorts of cell—nerve cells, stomach cells, cells of the respiratory lining—the virus can most effectively penetrate, and therefore what sort of disease it may cause. Useful as they are to a virus, though, the spikes also represent points of vulnerability. They are the primary targets of immune response by an infected host. Antibodies, produced by white blood cells, are molecules that glom onto the spikes and prevent a virion from grabbing a cell.
The capsid shouldn’t be mistaken for a cell wall or a cell membrane. It’s merely analogous. Viruses, from the beginning of virology, have been defined in the negative (not captured by a filter, not cultivable in chemical nutrients, not quite alive), and the most fundamental negative axiom is that a virion is not a cell. It doesn’t function the way a cell functions; it doesn’t share the same capacities or frailties. That’s reflected in the fact that viruses are impervious to antibiotics—chemicals valued for their ability to kill bacteria (which are cells) or at least impede their growth. Penicillin works by preventing bacteria from building their cell walls. So do its synthetic alternatives, such as amoxicillin. Tetracycline works by interfering with the internal metabolic processes by which bacteria manufacture new proteins for cell growth and replication. Viruses, lacking cell walls, lacking internal metabolic processes, are oblivious to the effects of such killer drugs.
Inside the viral capsid is usually nothing but genetic material, the set of instructions for creating new virions on the same pattern. Those instructions can only be implemented when they’re inserted into the works of a living cell. The material itself may be either DNA or RNA, depending on the family of virus. Both types of molecule are capable of recording and expressing information, though each has its advantages and its drawbacks. Herpesviruses, poxviruses, and papillomaviruses contain DNA; so do half a dozen viral families you’ve never heard of, such as the iridoviruses, the baculoviruses, and the hepadnaviruses (one of which causes hepatitis B). Others, including filoviruses, retroviruses (most notoriously, HIV-1), coronaviruses (SARS-CoV), and the families encompassing measles, mumps, Hendra, Nipah, yellow fever, dengue, West Nile, rabies, Machupo, Junin, Lassa, chikungunya, all the hantaviruses, all the influenzas, and the common cold viruses, store their genetic information in the form of RNA.
The different attributes of DNA and RNA account for one of the most crucial differences among viruses: rate of mutation. DNA is a double-stranded molecule, the famed double helix, and because its two strands fit together by way of those very specific relationships between pairs of nucleotide bases (adenine linking only with thymine, cytosine only with guanine), it generally repairs mistakes in the placement of bases as it replicates itself. This repair work is performed by DNA polymerase, the enzyme that helps catalyze construction of new DNA from single strands. If an adenine is mistakenly set in place to become linked with a guanine (not its correct partner), the polymerase recognizes that mistake, backtracks by one pair, fixes the mismatch, and then moves on. So the rate of mutation in most DNA viruses is relatively low. RNA viruses,