virus(redirected from rabies-like viruses)
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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.
virusInfectious disease A small, obligatorily intracellular agent ranging from 106 daltons–eg, Parvoviridae to 200 x 106–eg, Poxviridae; viral nucleic acid is single- or double-stranded, either DNA or RNA, and is a closed circle or opened and linear; viral nucleic acid is packaged within a protein coat–capsid composed of a few distinct types of protein; most have a helical or icosahedral symmetry; once inside the infected cell, the virus uses the host's synthetic capabilities to produce progeny virus; some viruses–eg, influenza virus, are 'studded' with external proteins–eg, hemagglutinins, neuraminidases
vi·rus, pl. viruses (vī'rŭs, -ĕz)
virus(vi'rus) [L. virus, poison]
Some of the most virulent diseases are caused by viruses, e.g., the hemorrhagic fever caused by Ebola virus. Viruses are also responsible for the common cold, childhood exanthems (such as chickenpox, measles, rubella), latent infections (such as herpes simplex), some cancers or lymphomas (such as Epstein-Barr virus), and diseases of all organ systems.
Although viral architecture is very complex, every virus contains at least a genome and a capsid.Most animal viruses are also surrounded by a lipid envelope, a bilayered membrane analogous to a cell membrane. The envelope may be parasitized from host cells. Its chemical components are phospholipids and glycoproteins. The lipid envelope is frequently dotted by spikes.
Viruses with lipid envelopes have a greater ability to adhere to cell membranes and to avoid destruction by the immune system. Both the capsid and envelope are antigenic. Frequent mutations change some viral antigens so that the lymphocytes are unable to create an antibody that can neutralize the original antigen and its replacement. The common influenza viruses have antigens that mutate or combine readily, requiring new vaccines with each mutation. The body's primary immune defenses against viruses are cytotoxic T lymphocytes, interferons, and, to some extent, immunoglobulins; destruction of the virus often requires destruction of the host cell.
When viruses enter a cell, they may immediately trigger a disease process or remain quiescent for years. They damage the host cell by blocking its normal protein synthesis and using its metabolic machinery for their own reproduction. New viruses are then released either by destroying their host cell or by forming small buds that break off and infect other cells. See: illustration; table
The 400 known viruses are classified in several ways: by genome core (RNA or DNA), host (animals, plants, or bacteria), method of reproduction (such as retrovirus), mode of transmission (such as enterovirus), and disease produced (such as hepatitis virus).
Antiviral drugs include such agents as acyclovir (for herpes simplex); oseltamivir and zanamivir (for influenza A); interferons (for chronic hepatitis B and C); ribavirin (for respiratory syncytial virus and chronic hepatitis C); and lamivudine (for HIV).
B virusCercopithecine herpesvirus 1.
Banna virusAbbreviation: BAV
Barmah Forest virus
cercopithecine virus 1Cercopithecine herpesvirus 1.
cowpea mosaic virus
coxsackie virusSee: coxsackievirus
cytomegalic virusAbbreviation: CMV
deer tick virus
delta hepatitis virusAbbreviation: HDV
See: hepatitis D
EB virusEpstein-Barr virus.
enteric cytopathogenic human orphan virusAbbreviation: echovirus
enteric orphan virusSee: enteric cytopathogenic human orphan virus
Epstein-Barr virusSee: Epstein-Barr virus
Eyach virusAbbreviation: EYAV
GB virus type CHepatitis G virus.
hepatitis G virus
herpes simplex virusAbbreviation: HSV-1, HSV-2
In immunosuppressed patients, the virus can cause a widely disseminated rash. Some infections with HSV may involve the brain and meninges; these typically cause fevers, headaches, altered mental status, seizures, or coma, requiring parenteral therapy with antiviral drugs. In newborns, infection involving the internal organs also may occur. Experienced ophthalmologists should manage ocular infection with HSVs. Health care providers are at risk for herpetic whitlow (finger infections) from contact with infected mucous membranes if gloves and meticulous hand hygiene are not used.
Acyclovir and related drugs, e.g., famciclovir, valacyclovir, may be used to treat outbreaks of HSV-1 and HSV-2 and are also effective in preventing recurrences of disease.
Standard precautions prevent spread of the virus. Prescribed antiviral agents and analgesics are administered; their use is explained to the patient, with instruction given about adverse effects to report.
The patient with HSV-1 is instructed to avoid skin-to-skin contact with uninfected individuals when lesions are present or prodromal symptoms are felt. To decrease the discomfort from oral lesions, the patient is advised to use a soft toothbrush or sponge stick, a saline- or bicarbonate-based (not alcohol-based) mouthwash, and oral anesthetics such as viscous lidocaine if necessary. He or she should eat soft foods. Use of lip balm with sunscreen reduces reactivation of oral lesions.
The patient with genital herpes should wash the hands carefully after bathroom use. He or she also should avoid sexual intercourse during the active stage of the disease and should practice safe sex. A pregnant woman must be advised of the potential risk to the infant during vaginal delivery and the use of cesarean delivery if she has an HSV outbreak when labor begins and her membranes have not ruptured. The patient with genital herpes may experience feelings of powerlessness. He requires assistance to identify coping mechanisms, strengths, and support resources; should be encouraged to voice feelings about perceived changes in sexuality and behavior; and should be provided with current information about the disease and treatment options. A referral is made for additional counseling as appropriate.
CAUTION!Caregivers with active oral or cutaneous lesions should avoid providing patient care.
herpes virusSee: herpesvirus
human immunodeficiency virusAbbreviation: HIV
human papilloma virusSee: papillomavirus
human T-cell lymphotropic virus type IAbbreviation: HTLV-I
human T-cell lymphotropic virus type IIAbbreviation: HTLV-II
human T-cell lymphotropic virus type IIIAbbreviation: HTLV-III
Inkoo virusAbbreviation: INK
Kyasanur Forest virus
Langat virusAbbreviation: LGT
Nipah virusAbbreviation: NiV
Norwalk virusAbbreviation: NLV
Omsk hemorrhagic fever virus
oncogenic virusTumor virus.
Puumala virusAbbreviation: PUUV
Rauscher leukemia virusSee: Rauscher leukemia virus
respiratory syncytial virusAbbreviation: RSV
Three to five days following exposure to RSV, the patient typically develops an upper respiratory infection lasting 1 to 2 weeks with cough, mild to moderate nasal congestion, runny nose, and low-grade fever. If the infection spreads to the lower respiratory tract, symptoms worsen and may include wheezing and difficulty breathing. Infants and children with RSV pneumonia exhibit retractions; rapid grunting respirations, poor oxygenation, and respiratory distress. Vomiting, dehydration, and acidosis may occur.
Diagnosis is based on signs and symptoms and confirmed by isolating RSV from respiratory secretions (sputum or throat swabs). Immunofluorescence techniques, enzyme immunoassays, or rapid chromatographic immunoassays provide rapid identification of viral antigens for diagnosis.
Treatment is mainly supportive. Antibiotics are not effective. Acetaminophen or ibuprofen are given for pain or fever. Oxygen is administered if the patient’s oxygen saturation SpO2 falls below 92%. Bronchodilators, such as albuterol and epinephrine, are used to treat wheezing. In patients with severe RSV infections, noninvasive positive-pressure ventilation or intubation and mechanic ventilation are required. Intravenous fluids are administered as prescribed if the patient cannot take enough fluid orally. Nasopharyngeal suction may be needed to clear congestion (by bulb syringe for infants).
Strict adherence to infection control measures is important in preventing an outbreak in any facility. This includes using meticulous hand hygiene (the most important step in preventing RSV spread) before donning gloves for patient care, after removing gloves, and if any potentially contaminated surfaces have been touched. Standard and contact precautions should be observed for all patients with known or suspected RSV (gown, mask and eye protection for direct contact with respiratory secretions or droplets). Protective coverings should be removed in this order: gloves (followed by hand hygiene), goggles or face shield, gown, and finally mask or respirator, discarding them in an infectious waste container in the patient’s room. The patient with RSV should be in a private room and dedicated equipment should be used in patient care, with terminal equipment disinfection by the appropriate agency facility. Room assignments should be arranged to avoid cross-contamination whenever possible. Individuals with symptoms of respiratory infection should be prevented from caring for or visiting pediatric, immunocompromised, or cardiac patients.
The administration of high doses of respiratory syncytial virus immune globulin is an effective means of preventing lower respiratory tract infection in infants and young children at high risk for contracting this disease. Palivizumab, a monoclonal antibody given intramuscularly, can prevent RSV disease in high-risk infants and children.
Rift Valley virus
Ross River virus
sandfly fever virusToscana virus
Serra do Navio virusAbbreviation: SDNV
simian immunodeficiency virus
SV 40 virus
Tacaribe complex virus
Tahyna virusAbbreviation: TAH
transfusion-transmissible virusAbbreviation: TTV
West Nile virus
In 2009 45 states in the U.S. reported having human cases of West Nile fever. There were 720 reported cases of this viral infection in the U.S. in 2009 and 32 fatalities. Infected patients with neuroinvasive disease sometimes suffer long-term consequences of infection, including fatigue and malaise, difficulty concentrating or thinking, or movement disorders. The disease is sometimes spread from patient to patient by blood transfusion or organ transplantation.
Disease transmission can be prevented with mosquito control and mosquito avoidance measures. Health care professionals should advise patients and families to limit time out of doors, esp. at dusk and dawn, to wear protective clothing (long sleeves, long pants, and socks), to place mosquito netting over infant carriers or strollers, and to apply an FDA-approved insect repellant (e.g., DEET, picaridin, or oil of lemon eucalyptus). Mosquito breeding grounds should be eliminated: standing water should be removed from flower pots, bird baths, pool covers, rain gutters, and discarded tires. Window and door screens should be installed and kept in good repair to prevent mosquitoes from entering homes.
xenotropic murine leukemia virus–related virusAbbreviation: XMRV virus
|RNA||HIV, hepatitis A, polio, measles, mumps, rhinovirus, influenza|
|DNA||Herpesviruses, hepatitis B, adenoviruses, human papilloma viruses, cytomegalovirus|
|Humans||Measles, mumps, rubella, varicella-zoster, poliovirus|
|Humans and animals||Rabies, influenza, hantavirus, encephalitis virus|
|Plants||Tobacco mosaic virus, cowpea mosaic virus|
|Present||Herpesviruses, rabies, HIV|
|Absent||Rotavirus, Norwalk virus, adenovirus|
|Respiratory||Influenza, parainfluenza, hantavirus|
|Teratogenic||Varicella-zoster virus, cytomegalovirus, rubella|
|Neurological and fatal||Rabies|
|Paralytic encephalitic||Polio, many encephalitis viruses|
|Fulminant||Yellow fever, hantavirus, Ebola-Marburg|
|Cancer causing||Human T-cell lymphotrophic virus, hepatitis viruses, papillomavirus|
virusa submicroscopic intracellular parasite, ranging in size from about 0.025 μ m to 0.25 μ m. The mature virus, a virion, consists of nucleic acid (RNA or DNA, which can be single-stranded or double-stranded, circular, linear or in separate segments, see SEGMENTED GENOME) surrounded by a coat of protein (capsid). In some viruses this is surrounded by an envelope of lipids, proteins and carbohydrates, and there may be spikes. Viruses infect cells of microorganisms, plants and animals, and whilst they carry out no METABOLISM themselves, they are able to control the metabolism of the infected cell. In infection the virus interacts with the host cell surface, and penetrates the cell. Virus nucleic acid is replicated and virus components are synthesized inside the cell. The newly formed virions are released from the cell.
vi·rus, pl. viruses (vī'rŭs, -ĕz)
Patient discussion about virus
Q. Is there a connection between Epstein-Barr Virus and Fibromyalgia and where can I find information? I was diagnosed with EBV 10 years ago and got diagnosed with Fibromyalgia and Depression 5 yrs ago-is there a connection and if so where can I obtain information. If anyone can help-Thank You!
Q. can an HIV virus last when it comes in contact with air and out of the body? in what ways can i get HIV? and what are the treatment options ? is it treatable ? and what are the side effects for this kind of treatment ?
http://en.wikipedia.org/wiki/HIV Hope this helps.
Q. One of my uncle is recovering from the flu and lower back pain. The flu was short... One of my uncle is recovering from the flu and lower back pain. The flu was short lived - this past saturday and super bowl sunday. He felt much better on Monday and worked half a day. Monday night the pain in his back started and he thought he must have twisted wrong somehow. He took a hot bath and went to bed. The next morning, He couldn't move. He immediately went to the doctor. The doctor was a bit puzzled by the pain, but not surpised by it, because of the flu. He said there is definitely a correlation. He was completely debilitated for one entire day, laying on the floor in each room of his house. He was given an inflamatory pill and a muscle relaxer. One day later, today, He is 25% better, which tells him that its a virus and not because he pulled something. He can walk a bit without pain and know tomorrow will be even better. To all who have this problem - Hang in there! and please help!