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Unlike cellular organisms, viruses do not contain all the biochemical mechanisms for their own replication; they replicate by using the biochemical mechanisms of a host cell to synthesize and assemble their separate components. (Some do contain or produce essential enzymes when there is no cellular enzyme that will serve.) When a complete virus particle (virion) comes in contact with a host cell, only the viral nucleic acid and, in some viruses, a few enzymes are injected into the host cell.
Within the host cell the genetic material of a DNA virus is replicated and transcribed into messenger RNA by host cell enzymes, and proteins coded for by viral genes are synthesized by host cell ribosomes. These are the proteins that form the capsid (protein coat); there may also be a few enzymes or regulatory proteins involved in assembling the capsid around newly synthesized viral nucleic acid, in controlling the biochemical mechanisms of the host cell, and in lysing the host cell when new virions have been assembled. Some of these may already have been present within the initial virus, and others may be coded for by the viral genome for production within the host cell.
Because host cells do not have the ability to replicate “viral RNA” but are able to transcribe messenger RNA, RNA viruses must contain enzymes to produce genetic material for new virions. For certain viruses the RNA is replicated by a viral enzyme (transcriptase) contained in the virion, or produced by the host cell using the viral RNA as a messenger. In other viruses a reverse transcriptase contained in the virion transcribes the genetic message on the viral RNA into DNA, which is then replicated by the host cell. Reverse transcriptase is actually a combination of two enzymes: a polymerase that assembles the new DNA copy and an RNase that degrades the source RNA.
In viruses that have membranes, membrane-bound viral proteins are synthesized by the host cell and move, like host cell membrane proteins, to the cell surface. When these proteins assemble to form the capsid, part of the host cell membrane is pinched off to form the envelope of the virion.
Some viruses have only a few genes coding for capsid proteins. Other more complex ones may have a few hundred genes. But no virus has the thousands of genes required by even the simplest cells. Although in general viruses “steal” their lipid envelope from the host cell, virtually all of them produce “envelope proteins” that penetrate the envelope and serve as receptors. Some envelope proteins facilitate viral entry into the cell, and others have directly pathogenic effects.
Some viruses do not produce rapid lysis of host cells, but rather remain latent for long periods in the host before the appearance of clinical symptoms. This carrier state can take any of several different forms. The term latency is used to denote the interval from infection to clinical manifestations. In the lentiviruses, it was formerly mistakenly believed that virus was inactive during this period. The true situation is that lentiviruses are rapidly replicating and spawning dozens of quasi-species until a particularly effective one overruns the ability of the host's immune system to defeat it. Other viruses, however, such as the herpesviruses, actually enter a time known as “viral latency,” when little or no replication is taking place until further replication is initiated by a specific trigger. For many years all forms of latency were thought to be identical, but now it has been discovered that there are different types with basic and important distinctions.
In viral latency, most of the host cells may be protected from infection by immune mechanisms involving antibodies to the viral particles or interferon. Cell-mediated immunity is essential, especially in dealing with infected host cells. Cytotoxic lymphocytes may also act as antigen-presenting cells to better coordinate the immune response. Containment of virus in mucosal tissues is far more complex, involving follicular dendritic cells and Langerhans cells.
Some enveloped RNA viruses can be produced in infected cells that continue growing and dividing without being killed. This probably involves some sort of intracellular regulation of viral growth. It is also possible for the DNA of some viruses to be incorporated into the host cell DNA, producing a carrier state. These are almost always retroviruses, which are called proviruses before and after integration of viral DNA into the host genome.
Few viruses produce toxins, although viral infections of bacteria can cause previously innocuous bacteria to become much more pathogenic and toxic. Other viral proteins, such as some of the human immunodeficiency virus, appear to be actively toxic, but those are the exception, not the rule.
However, viruses are highly antigenic. Mechanisms of pathologic injury to cells include cell lysis; induction of cell proliferation (as in certain warts and molluscum contagiosum); formation of giant cells, syncytia, or intracellular inclusion bodies caused by the virus; and perhaps most importantly, symptoms caused by the host's immune response, such as inflammation or the deposition of antigen-antibody complexes in tissues.
Because viral reproduction is almost completely carried out by host cell mechanisms, there are few points in the process where stopping viral reproduction will not also kill host cells. For this reason there are no chemotherapeutic agents for most viral diseases. acyclovir is an antiviral that requires viral proteins to become active. Some viral infections can be prevented by vaccination (active immunization), and others can be treated by passive immunization with immune globulin, although this has been shown to be effective against only a few dozen viruses.
HAVhepatitis A virus.
HAVHepatitis A virus, see there.
hallux abductovalgus; HAV biplanar first-ray deformity, where the tip of the hallux is deviated on the transverse plane (away from body midline) in conjunction with frontal-plane axial rotation of the hallux about its longitudinal axis (i.e. the medial nail sulcus approaches the support surface) and transverse-plane deviation of the first metatarsal head towards the midline of the body (i.e. secondary to metatarsus primus varus); HAV is associated with a range of forefoot pathologies (Table 1 and Box 1; Figure 1) and may require surgical correction Table 2
|Intrinsic to the foot and lower limb||Excess STJ and MTJ pronation||Ankle equinus|
Metatarsus primus elevatus
Metatarsus primus varus
Long second metatarsal/short first metatarsal
Functional hallux limitus
|Structural anomalies within the lower limb that predispose to compensatory foot pronation||External tibial torsion|
Genu varum/valgum, recurvatum
|Trauma||First MTPJ intra-articular damage|
First MTPJ sprain (turf toe)
Subluxed second toe
|Extrinsic to the foot and lower limb||Inflammatory joint disease||Rheumatoid disease|
|Connective tissue disorders characterized by joint hypermobility||Generalized hypermobility syndrome|
|Neuromuscular disease characterized by the development of pes cavus or pes planovalgus||Multiple sclerosis|
Hereditary sensorimotor neuropathy (Charcot–Marie–Tooth disease)
STJ, subtalar joint; MTJ, metatarsal joint; MTPJ, metatarsophalangeal joint.
|Good||The sheet of paper remains static and in situ when pulled|
|Fair||The sheet of paper moves slightly when pulled, but tends to tear when greater traction is applied|
|Poor||The sheet of paper can be pulled out with minimum effort|
|Absent||The paper slips out easily; it is not retained by the hallux as the pulp of the toe does not make ground contact|
Hallux purchase is inferred by the ease with which a sheet of paper can be pulled out from beneath the pulp of the weight-bearing hallux.
|Surgical approach||Intervention||Example procedure|
|Joint-destructive procedures||Excision of base of hallux proximal phalanx|
|Joint-preserving procedures||Closing basal wedge osteotomy, first metatarsal|
Distal metatarsal osteotomy
|Basal wedge osteotomy|
|Ray alignment procedures||Z osteotomy|
Medial closing-wedge osteotomy, hallux
|Ray stabilization procedures||Arthrodesis of first metatarsal/medial cuneiform joint||Lapidus|
|Cosmesis||Excision of medial eminence at head of first metatarsal (cheilectomy)||Silver|
There are over 100 named surgical techniques for the correction of hallux abductovalgus, most of which are modifications of a number of principles of approach.