Central Nervous System Viral Diseases
Central Nervous System
Central Nervous System Diseases
Central Nervous System Neoplasms
Nervous System
Brain
Central Nervous System Infections
Pseudorabies virus expressing bovine herpesvirus 1 glycoprotein B exhibits altered neurotropism and increased neurovirulence. (1/130)
Herpesvirus glycoproteins play dominant roles in the initiation of infection of target cells in culture and thus may also influence viral tropism in vivo. Whereas the relative contribution of several nonessential glycoproteins to neurovirulence and neurotropism of Pseudorabies virus (PrV), an alphaherpesvirus which causes Aujeszky's disease in pigs, has recently been uncovered in studies using viral deletion mutants, the importance of essential glycoproteins is more difficult to assess. We isolated an infectious PrV mutant, PrV-9112C2, which lacks the gene encoding the essential PrV glycoprotein B (gB) but stably carries in its genome and expresses the homologous gene of bovine herpesvirus 1 (BHV-1) (A. Kopp and T. C. Mettenleiter, J. Virol. 66:2754-2762, 1992). Apart from exhibiting a slight delay in penetration kinetics, PrV-9112C2 was similar in its growth characteristics in cell culture to wild-type PrV. To analyze the effect of the exchange of these homologous glycoproteins in PrV's natural host, swine, 4-week-old piglets were intranasally infected with 10(6) PFU of either wild-type PrV strain Kaplan (PrV-Ka), PrV-9112C2, or PrV-9112C2R, in which the PrV gB gene was reinserted instead of the BHV-1 gB gene. Animals infected with PrV-Ka and PrV-9112C2R showed a similar course of disease, i.e., high fever, marked respiratory symptoms but minimal neurological disorders, and excretion of high amounts of virus. All animals survived the infection. In contrast, animals infected with PrV-9112C2 showed no respiratory symptoms and developed only mild fever. However, on day 5 after infection, all piglets developed severe central nervous system (CNS) symptoms leading to death within 48 to 72 h. Detailed histological analyses showed that PrV-9112C2R infected all regions of the nasal mucosa and subsequently spread to the CNS preferentially by the trigeminal route. In contrast, PrV-9112C2 primarily infected the olfactory epithelium and spread via the olfactory route. In the CNS, more viral antigen and significantly more pronounced histological changes resulting in more severe encephalitis were found after PrV-9112C2 infection. Thus, our results demonstrate that replacement of PrV gB by the homologous BHV-1 glycoprotein resulted in a dramatic increase in neurovirulence combined with an alteration in the route of neuroinvasion, indicating that the essential gB is involved in determining neurotropism and neurovirulence of PrV. (+info)Role of pseudorabies virus Us9, a type II membrane protein, in infection of tissue culture cells and the rat nervous system. (2/130)
The protein product of the pseudorabies virus (PRV) Us9 gene is a phosphorylated, type II membrane protein that is inserted into virion envelopes and accumulates in the trans-Golgi network. It is among a linked group of three envelope protein genes in the unique short region of the PRV genome which are absent from the attenuated Bartha strain. We found that two different Us9 null mutants exhibited no obvious phenotype after infection of PK15 cells in culture. Unlike those of gE and gI null mutants, the plaque size of Us9 null mutants on Madin-Darby bovine kidney cells was indistinguishable from that of wild-type virus. However, both of the Us9 null mutants exhibited a defect in anterograde spread in the visual and cortical circuitry of the rat. The visual system defect was characterized by restricted infection of a functionally distinct subset of visual projections involved in the temporal organization of behavior, whereas decreased anterograde spread of virus to the cortical projection targets was characteristic of animals receiving direct injections of virus into the cortex. Spread of virus through retrograde pathways in the brain was not compromised by a Us9 deletion. The virulence of the Us9 null mutants, as measured by time to death and appearance of symptoms of infection, also was reduced after their injection into the eye, but not after cortical injection. Through sequence analysis, construction of revertants, measurement of gE and gI protein synthesis in the Us9 null mutants, and mixed-infection studies of rats, we conclude that the restricted-spread phenotype after infection of the rat nervous system reflects the loss of Us9 and is not an indirect effect of the Us9 mutations on expression of glycoproteins gE and gI. Therefore, at least three viral envelope proteins, Us9, gE, and gI, function together to promote efficient anterograde transneuronal infection by PRV in the rat central nervous system. (+info)Antiretroviral resistance mutations in human immunodeficiency virus type 1 reverse transcriptase and protease from paired cerebrospinal fluid and plasma samples. (3/130)
Twenty-four adults infected with human immunodeficiency virus type 1 (HIV-1) with central nervous system symptoms were studied for antiretroviral resistance mutations in HIV-1 RNA obtained from paired cerebrospinal fluid (CSF) and plasma samples. Paired sequences were obtained from 21 and 13 patients for reverse transcriptase (RT) and for protease, respectively. Mutations conferring resistance to the RT inhibitors zidovudine, lamivudine, or nevirapine were detected in 14 patients, including 11 pretreated and 3 drug-naive subjects. The mutation patterns in the 2 compartments were different in most patients. Genotypic resistance to protease inhibitors was detected in both plasma and CSF from 1 patient treated with multiple protease inhibitors. However, accessory protease inhibitor resistance mutations at polymorphic sites were different in plasma and CSF in several patients. Partially independent evolution of viral quasispecies occurs in plasma and CSF, raising the possibility that compartmentalization of drug resistance may affect response to antiretroviral treatment. (+info)Synaptic pathology in Borna disease virus persistent infection. (4/130)
Borna disease virus (BDV) infection of newborn rats leads to a persistent infection of the brain, which is associated with behavioral and neuroanatonomical abnormalities. These disorders occur in the absence of lymphoid cell infiltrates, and BDV-induced cell damage is restricted to defined brain areas. To investigate if damage to synaptic structures anteceded neuronal loss in BDV neonatally infected rats, we analyzed at different times postinfection the expression levels of growth-associated protein 43 and synaptophysin, two molecules involved in neuroplasticity processes. We found that BDV induced a progressive and marked decrease in the expression of these synaptic markers, which was followed by a significant loss of cortical neurons. Our findings suggest that BDV persistent infection interferes with neuroplasticity processes in specific cell populations. This, in turn, could affect the proper supply of growth factors and other molecules required for survival of selective neuronal populations within the cortex and limbic system structures. (+info)Control of Sindbis virus infection by antibody in interferon-deficient mice. (5/130)
Antibodies clear Sindbis virus from infected animals through an unknown mechanism. To determine whether interferon-induced pathways are required for this clearance, we examined mice which are unable to respond to alpha/beta interferon or gamma interferon. Although extremely susceptible to infection, such mice survived and completely cleared virus if antibodies against Sindbis virus were given. (+info)A molecular clone of simian-human immunodeficiency virus (DeltavpuSHIV(KU-1bMC33)) with a truncated, non-membrane-bound vpu results in rapid CD4(+) T cell loss and neuro-AIDS in pig-tailed macaques. (6/130)
We report on the role of vpu in the pathogenesis of a molecularly cloned simian-human immunodeficiency virus (SHIV(KU-1bMC33)), in which the tat, rev, vpu, env, and nef genes derived from the uncloned SHIV(KU-1b) virus were inserted into the genetic background of parental nonpathogenic SHIV-4. A mutant was constructed (DeltavpuSHIV(KU-1bMC33)) in which 42 of 82 amino acids of Vpu were deleted. Phase partitioning studies revealed that the truncated Vpu was not an integral membrane protein, and pulse-chase culture studies revealed that cells inoculated with DeltavpuSHIV(KU-1bMC33) released viral p27 into the culture medium with slightly reduced kinetics compared with cultures inoculated with SHIV(KU-1bMC33). Inoculation of DeltavpuSHIV(KU-1bMC33) into two pig-tailed macaques resulted in a severe decline of CD4(+) T cells and neurological disease in one macaque and a more moderate decline of CD4(+) T cells in the other macaque. These results indicate that a membrane-bound Vpu is not required for the CD4(+) T cell loss and neurological disease in SHIV-inoculated pig-tailed macaques. Furthermore, because the amino acid substitutions in the Tat and Rev were identical to those previously reported for the nonpathogenic SHIV(PPc), our results indicate that amino acid substitutions in the Env and/or Nef were responsible for the observed CD4(+) T cell loss and neurological disease after inoculation with this molecular clone. (+info)Detection of Herpes simplex virus DNA by real-time PCR. (7/130)
Molecular detection of herpes simplex virus (HSV) DNA is recognized as the reference standard assay method for the sensitive and specific diagnosis of central nervous system infections caused by HSV. In this study, a molecular assay based on real-time PCR on the LightCycler (LC) instrument was evaluated and compared with a home-brew molecular assay. The detection limit of the LC assay was determined with 10-fold dilutions of plasmid pS4 with the SalI restriction fragment of the DNA polymerase gene and with the First European Union Concerted Action HSV Proficiency Panel. A total of 59 cerebrospinal fluid (CSF) specimens were investigated for the comparative study. With plasmid pS4, the detection limit of the LC assay was found to be 10(4) copies per ml, i.e., 12.5 copies per run. When samples of the First European Union Concerted Action HSV Proficiency Panel were tested, 2x10(3) to 5x10(3) HSV type 1 genome equivalents (GE) per ml, i.e., 2.5 to 6.3 GE per run, could consistently be detected. There was a correlation between the LC assay and the home-brew assay in 55 of 59 specimens. In conclusion, the LC assay allows very rapid detection of HSV DNA in CSF. It was found to be laborsaving and showed sufficient sensitivity. (+info)Neurological symptoms during primary human immunodeficiency virus (HIV) infection correlate with high levels of HIV RNA in cerebrospinal fluid. (8/130)
This analysis involves 22 patients with diagnosed symptomatic human immunodeficiency virus (HIV) infection. Neurologic symptoms were present in 11 patients, ranging from severe and persistent headache to clinical signs suggestive of meningitis. A strong correlation between neurological symptoms and cerebrospinal fluid (CSF) viral load was found. The mean CSF HIV ribonucleic acid (RNA) level was 4. 12 log for patients with neurological symptoms and 2.58 log for patients without neurological symptoms (P<.00001). Plasma viral load alone does not correlate or predict central nervous system (CNS) involvement. In our sample of patients, HIV RNA levels could be detected in most patients regardless of the presence of neurological symptoms. Moreover, early treatment including drugs with high levels of penetration in the CNS must be considered for patients with primary HIV infection. (+info)Central nervous system (CNS) viral diseases refer to medical conditions caused by the infection and replication of viruses within the brain or spinal cord. These viruses can cause a range of symptoms, depending on the specific virus and the location of the infection within the CNS. Some common examples of CNS viral diseases include:
1. Meningitis: This is an inflammation of the membranes surrounding the brain and spinal cord (meninges) caused by viruses such as enteroviruses, herpes simplex virus, or HIV. Symptoms may include fever, headache, stiff neck, and altered mental status.
2. Encephalitis: This is an inflammation of the brain parenchyma caused by viruses such as herpes simplex virus, West Nile virus, or rabies virus. Symptoms may include fever, headache, confusion, seizures, and focal neurologic deficits.
3. Poliomyelitis: This is a highly infectious disease caused by the poliovirus that can lead to paralysis of the muscles used for breathing, swallowing, and movement. It primarily affects children under 5 years old.
4. HIV-associated neurological disorders (HAND): HIV can cause various neurologic symptoms such as cognitive impairment, peripheral neuropathy, and myopathy.
5. Progressive multifocal leukoencephalopathy (PML): This is a rare but serious demyelinating disease of the CNS caused by the JC virus that primarily affects individuals with weakened immune systems, such as those with HIV/AIDS or those receiving immunosuppressive therapy.
Treatment for CNS viral diseases depends on the specific virus and may include antiviral medications, supportive care, and management of symptoms. Prevention measures such as vaccination, avoiding contact with infected individuals, and practicing good hygiene can help reduce the risk of these infections.
The Central Nervous System (CNS) is the part of the nervous system that consists of the brain and spinal cord. It is called the "central" system because it receives information from, and sends information to, the rest of the body through peripheral nerves, which make up the Peripheral Nervous System (PNS).
The CNS is responsible for processing sensory information, controlling motor functions, and regulating various autonomic processes like heart rate, respiration, and digestion. The brain, as the command center of the CNS, interprets sensory stimuli, formulates thoughts, and initiates actions. The spinal cord serves as a conduit for nerve impulses traveling to and from the brain and the rest of the body.
The CNS is protected by several structures, including the skull (which houses the brain) and the vertebral column (which surrounds and protects the spinal cord). Despite these protective measures, the CNS remains vulnerable to injury and disease, which can have severe consequences due to its crucial role in controlling essential bodily functions.
Central nervous system (CNS) diseases refer to medical conditions that primarily affect the brain and spinal cord. The CNS is responsible for controlling various functions in the body, including movement, sensation, cognition, and behavior. Therefore, diseases of the CNS can have significant impacts on a person's quality of life and overall health.
There are many different types of CNS diseases, including:
1. Infectious diseases: These are caused by viruses, bacteria, fungi, or parasites that infect the brain or spinal cord. Examples include meningitis, encephalitis, and polio.
2. Neurodegenerative diseases: These are characterized by progressive loss of nerve cells in the brain or spinal cord. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
3. Structural diseases: These involve damage to the physical structure of the brain or spinal cord, such as from trauma, tumors, or stroke.
4. Functional diseases: These affect the function of the nervous system without obvious structural damage, such as multiple sclerosis and epilepsy.
5. Genetic disorders: Some CNS diseases are caused by genetic mutations, such as spinal muscular atrophy and Friedreich's ataxia.
Symptoms of CNS diseases can vary widely depending on the specific condition and the area of the brain or spinal cord that is affected. They may include muscle weakness, paralysis, seizures, loss of sensation, difficulty with coordination and balance, confusion, memory loss, changes in behavior or mood, and pain. Treatment for CNS diseases depends on the specific condition and may involve medications, surgery, rehabilitation therapy, or a combination of these approaches.
Viral diseases are illnesses caused by the infection and replication of viruses in host organisms. These infectious agents are obligate parasites, meaning they rely on the cells of other living organisms to survive and reproduce. Viruses can infect various types of hosts, including animals, plants, and microorganisms, causing a wide range of diseases with varying symptoms and severity.
Once a virus enters a host cell, it takes over the cell's machinery to produce new viral particles, often leading to cell damage or death. The immune system recognizes the viral components as foreign and mounts an immune response to eliminate the infection. This response can result in inflammation, fever, and other symptoms associated with viral diseases.
Examples of well-known viral diseases include:
1. Influenza (flu) - caused by influenza A, B, or C viruses
2. Common cold - usually caused by rhinoviruses or coronaviruses
3. HIV/AIDS - caused by human immunodeficiency virus (HIV)
4. Measles - caused by measles morbillivirus
5. Hepatitis B and C - caused by hepatitis B virus (HBV) and hepatitis C virus (HCV), respectively
6. Herpes simplex - caused by herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2)
7. Chickenpox and shingles - both caused by varicella-zoster virus (VZV)
8. Rabies - caused by rabies lyssavirus
9. Ebola - caused by ebolaviruses
10. COVID-19 - caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Prevention and treatment strategies for viral diseases may include vaccination, antiviral medications, and supportive care to manage symptoms while the immune system fights off the infection.
Central nervous system (CNS) neoplasms refer to a group of abnormal growths or tumors that develop within the brain or spinal cord. These tumors can be benign or malignant, and their growth can compress or disrupt the normal functioning of surrounding brain or spinal cord tissue.
Benign CNS neoplasms are slow-growing and rarely spread to other parts of the body. However, they can still cause significant problems if they grow large enough to put pressure on vital structures within the brain or spinal cord. Malignant CNS neoplasms, on the other hand, are aggressive tumors that can invade and destroy surrounding tissue. They may also spread to other parts of the CNS or, rarely, to other organs in the body.
CNS neoplasms can arise from various types of cells within the brain or spinal cord, including nerve cells, glial cells (which provide support and insulation for nerve cells), and supportive tissues such as blood vessels. The specific type of CNS neoplasm is often used to help guide treatment decisions and determine prognosis.
Symptoms of CNS neoplasms can vary widely depending on the location and size of the tumor, but may include headaches, seizures, weakness or paralysis, vision or hearing changes, balance problems, memory loss, and changes in behavior or personality. Treatment options for CNS neoplasms may include surgery, radiation therapy, chemotherapy, or a combination of these approaches.
The nervous system is a complex, highly organized network of specialized cells called neurons and glial cells that communicate with each other via electrical and chemical signals to coordinate various functions and activities in the body. It consists of two main parts: the central nervous system (CNS), including the brain and spinal cord, and the peripheral nervous system (PNS), which includes all the nerves and ganglia outside the CNS.
The primary function of the nervous system is to receive, process, and integrate information from both internal and external environments and then respond by generating appropriate motor outputs or behaviors. This involves sensing various stimuli through specialized receptors, transmitting this information through afferent neurons to the CNS for processing, integrating this information with other inputs and memories, making decisions based on this processed information, and finally executing responses through efferent neurons that control effector organs such as muscles and glands.
The nervous system can be further divided into subsystems based on their functions, including the somatic nervous system, which controls voluntary movements and reflexes; the autonomic nervous system, which regulates involuntary physiological processes like heart rate, digestion, and respiration; and the enteric nervous system, which is a specialized subset of the autonomic nervous system that controls gut functions. Overall, the nervous system plays a critical role in maintaining homeostasis, regulating behavior, and enabling cognition and consciousness.
The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:
1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.
The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.
Central nervous system (CNS) infections refer to infectious processes that affect the brain, spinal cord, and their surrounding membranes, known as meninges. These infections can be caused by various microorganisms, including bacteria, viruses, fungi, and parasites. Examples of CNS infections are:
1. Meningitis: Inflammation of the meninges, usually caused by bacterial or viral infections. Bacterial meningitis is a medical emergency that requires immediate treatment.
2. Encephalitis: Inflammation of the brain parenchyma, often caused by viral infections. Some viruses associated with encephalitis include herpes simplex virus, enteroviruses, and arboviruses.
3. Meningoencephalitis: A combined inflammation of both the brain and meninges, commonly seen in certain viral infections or when bacterial pathogens directly invade the brain.
4. Brain abscess: A localized collection of pus within the brain caused by a bacterial or fungal infection.
5. Spinal epidural abscess: An infection in the space surrounding the spinal cord, usually caused by bacteria.
6. Myelitis: Inflammation of the spinal cord, which can result from viral, bacterial, or fungal infections.
7. Rarely, parasitic infections like toxoplasmosis and cysticercosis can also affect the CNS.
Symptoms of CNS infections may include fever, headache, stiff neck, altered mental status, seizures, focal neurological deficits, or meningeal signs (e.g., Brudzinski's and Kernig's signs). The specific symptoms depend on the location and extent of the infection, as well as the causative organism. Prompt diagnosis and treatment are crucial to prevent long-term neurological complications or death.
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