Entry can occur by direct penetration of the protein coat and insertion of the viral genome (polio and other nonenveloped viruses), fusion of the viral envelope with the host cell membrane (measles and mumps viruses) or by stimulation of endocytosis of the entire enveloped virus (herpes and the nonenveloped adenovirus).

Those viruses that penetrate via membrane fusion and endocytosis must then undergo uncoating, either in the cytoplasm orwhile within the endocytitic vesicle.  The host cell's own enzymes cause this to occur, though the mechanism that triggers this process is not well understood.

dsDNA Virus Replication

dsDNA forms such as herpes and papilloma viruses use this strategy.  Pox viruses replicate in the cytoplasm only, while the genome of hepatitis B is first transcribed to RNA, then the RNA template is used to generate new dsDNA using reverse transcriptase, an enzyme carried by the virus.

ssDNA Replication

ssDNA forms, such as the parvovirus replicate using this strategy.  The replication of the complementary strand occurs in the nucleus, but the complementary strand is not incorporated into the nucleocapsid during assembly.


The (+) ssRNA viruses such as polio and rhinoviruses have RNA that can act immediately as mRNA to synthesize viral proteins.  New (+) strands are synthesized from a (-) strand, then assembled as nucleocapsids prior to release.


(-)ssRNA viruses such as filoviruses, reoviruses and arenaviruses must first synthesize a new (+) strand following uncoating.  The (+) strand can then be used to synthesize new complementary (-) strands and as mRNA to synthesize viral proteins.



Release of Animal Viruses

Nonenveloped viruses are released by cell lysis, but enveloped forms are released by budding.  Budding occurs when the nucleocapsid migrates to and is surrounded by a portion of host cell membrane from either the nucleus, endoplasmic reticulum or outer membrane.  During synthesis, viral protein spikes such as neuraminidase and hemagluttinin are added to the host membrane.

Latency and Persistance in Animal Viruses

Some animal viruses such as Herpes Zoster (chickenpox, shingles), Herpes Simplex I and II and HIV have the ability to remain in the body for extended periods of time without expressing themselves in a lytic cycle.  The process, called latency, occurs two ways:

Herpes viruses produce lytic cycles when infecting mucosal or epithelial cells, but have the ability to reside in the ganglia of nervous tissues without killing the cells, migrating to the cells they are specific for after being stimulated by some environmental factor such as exposure to radiation or by lowering of resistance due to another disorder (gastroenteritis, influenza, AIDS).

The HIV virus becomes a provirus (viral DNA incorporated with a host cell chromosome) and is held inactive by a repressor protein for long periods of time.  Stimulated by environmental or host stimuli as above, the proviral DNA is used to transcribe viral RNA, which begins the replication cycle.

Persistant viruses are those that are retained in the body in small numbers that continually replicate.  The accumulation of tissue damage over long periods of time plays a major role in pathogenicity.  Measles viruses, for example, can persist in nervous tissue for decades, eventually leading to a disorder called subacute schlerosing panencephalitis.