https://en.wikipedia.org/wiki/Thumps
Category A[edit]
These high-priority agents pose a risk to national security, can be easily transmitted and disseminated, result in high mortality, have potential major public health impact, may cause public panic, or require special action for public health preparedness.
SARS, though not as lethal as other diseases, was concerning to scientists[19][20] and policymakers for its social and economic disruption potential.[21] After the global containment of the pandemic, the United States President George W. Bush stated "...A global influenza pandemic that infects millions and lasts from one to three years could be far worse."[22]
Tularemia or "rabbit fever":[23] Tularemia has a very low fatality rate if treated, but can severely incapacitate. The disease is caused by the Francisella tularensis bacterium, and can be contracted through contact with fur, inhalation, ingestion of contaminated water or insect bites. Francisella tularensis is very infectious. A small number of organisms (10–50 or so) can cause disease. If F. tularensis were used as a weapon, the bacteria would likely be made airborne for exposure by inhalation. People who inhale an infectious aerosol would generally experience severe respiratory illness, including life-threatening pneumonia and systemic infection, if they are not treated. The bacteria that cause tularemia occur widely in nature and could be isolated and grown in quantity in a laboratory, although manufacturing an effective aerosol weapon would require considerable sophistication.[24]
Anthrax: Anthrax is a non-contagious disease caused by the spore-forming bacterium Bacillus anthracis. The ability of Anthrax to produce within small spores, or bacilli bacterium, makes it readily permeable to porous skin and can cause abrupt symptoms within 24 hours of exposure. The dispersal of this pathogen among densely populated areas is said to carry less than one percent mortality rate, for cutaneous exposure, to a ninety percent or higher mortality for untreated inhalational infections.[25] An anthrax vaccine does exist but requires many injections for stable use. When discovered early, anthrax can be cured by administering antibiotics (such as ciprofloxacin).[26] Its first modern incidence in biological warfare were when Scandinavian "freedom fighters" supplied by the German General Staff used anthrax with unknown results against the Imperial Russian Army in Finland in 1916.[27] In 1993, the Aum Shinrikyo used anthrax in an unsuccessful attempt in Tokyo with zero fatalities.[14] Anthrax was used in a series of attacks by a microbiologist at the US Army Medical Research Institute of Infection Disease on the offices of several United States Senators in late 2001. The anthrax was in a powder form and it was delivered by the mail.[28] This bioterrorist attack inevitably prompted seven cases of cutaneous anthrax and eleven cases of inhalation anthrax, with five leading to deaths. Additionally, an estimated 10 to 26 cases had prevented fatality through treatment supplied to over 30,000 individuals.[29] Anthrax is one of the few biological agents that federal employees have been vaccinated for. In the US an anthrax vaccine, Anthrax Vaccine Adsorbed (AVA) exists and requires five injections for stable use. Other anthrax vaccines also exist. The strain used in the 2001 anthrax attacks was identical to the strain used by the USAMRIID.[30]
Smallpox:[31] Smallpox is a highly contagious virus. It is transmitted easily through the atmosphere and has a high mortality rate (20–40%). Smallpox was eradicated in the world in the 1970s, thanks to a worldwide vaccination program.[32] However, some virus samples are still available in Russian and American laboratories. Some believe that after the collapse of the Soviet Union, cultures of smallpox have become available in other countries. Although people born pre-1970 will have been vaccinated for smallpox under the WHO program, the effectiveness of vaccination is limited since the vaccine provides high level of immunity for only 3 to 5 years. Revaccination's protection lasts longer.[33] As a biological weapon smallpox is dangerous because of the highly contagious nature of both the infected and their pox. Also, the infrequency with which vaccines are administered among the general population since the eradication of the disease would leave most people unprotected in the event of an outbreak. Smallpox occurs only in humans, and has no external hosts or vectors.
Botulinum toxin:[34] The neurotoxin[35] Botulinum is the deadliest toxin known to man, and is produced by the bacterium Clostridium botulinum. Botulism causes death by respiratory failure and paralysis.[36] Furthermore, the toxin is readily available worldwide due to its cosmetic applications in injections.
Bubonic plague:[37] Plague is a disease caused by the Yersinia pestis bacterium. Rodents are the normal host of plague, and the disease is transmitted to humans by flea bites and occasionally by aerosol in the form of pneumonic plague.[38] The disease has a history of use in biological warfare dating back many centuries, and is considered a threat due to its ease of culture and ability to remain in circulation among local rodents for a long period of time. The weaponized threat comes mainly in the form of pneumonic plague (infection by inhalation)[39] It was the disease that caused the Black Death in Medieval Europe.
Viral hemorrhagic fevers:[40] This includes hemorrhagic fevers caused by members of the family Filoviridae (Marburg virus and Ebola virus), and by the family Arenaviridae (for example Lassa virus and Machupo virus). Ebola virus disease, in particular, has caused high fatality rates ranging from 25 to 90% with a 50% average. No cure currently exists, although vaccines are in development. The Soviet Union investigated the use of filoviruses for biological warfare, and the Aum Shinrikyo group unsuccessfully attempted to obtain cultures of Ebola virus.[41] Death from Ebola virus disease is commonly due to multiple organ failure and hypovolemic shock. Marburg virus was first discovered in Marburg, Germany. No treatments currently exist aside from supportive care. The arenaviruses have a somewhat reduced case-fatality rate compared to disease caused by filoviruses, but are more widely distributed, chiefly in central Africa and South America.
Category B[edit]
Category B agents are moderately easy to disseminate and have low mortality rates.
Brucellosis (Brucella species)[42]
Epsilon toxin of Clostridium perfringens
Food safety threats (for example, Salmonella species, E coli O157:H7, Shigella, Staphylococcus aureus)
Glanders[43] (Burkholderia mallei)
Melioidosis (Burkholderia pseudomallei)[44][45]
Psittacosis (Chlamydia psittaci)
Q fever (Coxiella burnetii)[46]
Ricin[47] toxin from Ricinus communis (castor beans)
Abrin toxin from Abrus precatorius (Rosary peas)
Staphylococcal enterotoxin B
Typhus (Rickettsia prowazekii)
Viral encephalitis (alphaviruses, for example,: Venezuelan equine encephalitis, eastern equine encephalitis, western equine encephalitis)
Water supply threats (for example, Vibrio cholerae,[48] Cryptosporidium parvum)
Category C[edit]
Category C agents are emerging pathogens that might be engineered for mass dissemination because of their availability, ease of production and dissemination, high mortality rate, or ability to cause a major health impact.
Nipah virus
Hantavirus
https://en.wikipedia.org/wiki/Bioterrorism
David C. Goldman, in Principles and Practice of Pediatric Infectious Disease (Third Edition), 2008
Vaccinia Immune Globulin
Vaccinia IG (human) (VIG) was developed in the 1960s for the purpose of ameliorating side effects associated with vaccinia immunization, including eczema vaccinatum, generalized, and progressive vaccinia.48 The original preparation contained a high proportion of protein aggregates and thus was administered IM. The use of VIG has become extremely limited since the eradication of smallpox. It is considered valuable “insurance,” to be held in reserve if a patient is receiving an experimental vaccine that involves a vaccinia carrier virus, or to prevent or manage complications of smallpox vaccination should such be required for a bioterrorism threat. Recently, a preparation of VIG suitable for IV use (VIG-IGIV) has gained FDA approval. In the event that VIG is required, it can be obtained through the Centers for Disease Control and Prevention (CDC: www.bt.cdc.gov/agent/smallpox/).
https://www.sciencedirect.com/topics/medicine-and-dentistry/vaccinia
Evident in USAF and unco of CL1Grade Low Waste. Tissue scars eczema liquefies with anesthetic surg/pyrotics/phosphors/phos ders/solvents/genetic dissolution protein dissolution/nucleoradiation/etc.. infection asympto hidden by methroxetrate/alkali; they require alkali environment to stabilize, intolerant of acids (damage to nerves evident with reinnervation attempts or psuedosignal). MJ v. nothing; scrambled; vaccina or HIV or Acquired-Immunity (esp. in presence of nucleoradiation, over radiation environment, methroxetrate environment allergens etc.). small pox virus campaign 1920-1980. coverup USA petersens-usaf-usa-nac-etc. guilty as charged. Stronger than the man. Evident at UCLA, etc..
Evident at high risk criminals, petersen, smith, mx, hawaii, middle east, bruens, browns, norway, jew, aziv, layng, grayden, psychopath, criminals in conspiracy to traffick birthright, wade siboan, social work, USA, USAF, USAF, USA, NAC, US, psychology, sociology, criminal justice law, US law enforcement, inferior, inferior scientist, rebodied persons, double connect, indoctrinated, carried memory without appreciation, everyone except VIV/birthright/etc., clones, stolen child trafficker family, stolen child, trafficker, trafficker sympathizer, etc.. Conspiracy to cover up gross theft of intellectual property. Damages by USA are not excusable. VIV and birthright never of USA (enduring enhostage situation).
Diverse profile Winers
1. petersen profile - Phosphatidylethanolamine- lipodistrophy organ trans - HIV; Account - molluscum contagium, poxiviridae USA.
2. Dr. Beatles profile - sarcoma fibromatosis - EIE EIA; Account - Daughter end at USA.
3. CIVLEVEL - Overvaccination to progressive vaccina [unk civs], HyperImmune/anaphylaxis-rash-fever (subclinical/asymptomatic)/allergy/autoimmune disease-condition-etc./gen-dis/gen-mod/etc.-HIDS(huminal immune deficiency syndrome)-IDS (immune deficiency disease disorder dysfunction)/AIDS w/ or w/o HIV ssN negs vi, - Hyperimmunity downstepping etc.; etc.. Account - Illusion-Delusion-Disease-Deform-Dangerous-Disorder-Mental/Ill-InferiorGenetics-Denial USA; DEceit by USA, Conspiracy, Birthright victim of mass trafficking (missing parts, shell eyes etc.), scientist SSF enhostage, amnestic drug/cloak/technology advancement and pharmaceutical advancement not disclosed to General populace-world and where use by USA in manner as not intended by manuf./IP-origin-designer-eng-original-etc./etc./etc.. (one boyfriend overvaccinated)
Victims
MRI of the Bile Ducts, Gallbladder, and Pancreas
Saroja Adusumilli MD, Evan S. Siegelman MD, in Body MRI, 2005
AIDS CHOLANGIOPATHY
Acquired immunodeficiency syndrome (AIDS) can affect the biliary tree in one of two ways: infectious cholangiopathy or biliary obstruction secondary to extrinsic compression by periportal lymph nodes from AIDS-related lymphoma.116 AIDS cholangiopath is usually the result of bile infection by either Cytomegalovirus or Cryptosporidium. The imaging features of AIDS cholangiopathy include moderate biliary duct dilatation with irregular mural thickening and nodules, ampullary stenosis, and gallbladder sludge.116 Intrahepatic duct findings such as focal stenoses with segmental dilatation (“beaded” appearance) simulate primary sclerosing cholangitis. The extrahepatic duct abnormalities present in PSC such as saccules and high-grade strictures are not present in AIDS cholangiopathy.116
HIV and AIDS
Wang-Shick Ryu, in Molecular Virology of Human Pathogenic Viruses, 2017
As a consequence, opportunistic infections such as pneumonia occur and are the main cause of death of HIV infected patients.
Acquired Immune Deficiency Syndrome
Acquired immune deficiency syndrome (AIDS) occurs when an HIV-positive person's immune system is weakened, specifically when the T cell count drops below 200.
From: Encyclopedia of Adolescence, 2011
Related terms:
LesionKaposi SarcomaHuman Immunodeficiency VirusCytomegalovirusAntiretroviral TherapyHuman Immunodeficiency Virus 1Human Immunodeficiency Virus Infection
https://www.sciencedirect.com/topics/medicine-and-dentistry/acquired-immune-deficiency-syndrome
Poliomyelitis
Ondrej Mach, ... T. Jacob John, in International Encyclopedia of Public Health (Second Edition), 2017
Abstract
Poliomyelitis, an acute communicable disease affecting primarily children with the major manifestation of muscle paralysis, is caused by an enterovirus – poliovirus – with previously worldwide distribution. The development of first inactivated, and then attenuated, live poliovirus vaccines in the 1950s was an historic public health achievement of the twentieth century. Although polio has been eliminated from most of the world, as of June 2014, it remains endemic in three countries (Afghanistan, Pakistan, and Nigeria); and exportations of poliovirus into previously polio-free countries occur frequently, causing large outbreaks if the virus reaches areas with low population immunity.
Lessons about research ethics, the selection of appropriate vaccine types for different populations, and the importance of reducing unintended side effectssuch as vaccine virus–induced paralysis are highlighted in this article.
Polio
Donna J. Fisher MD, in Pediatric Clinical Advisor (Second Edition), 2007
Basic Information
Definition
Polio is an acute viral infection of the brainstem and spinal cord that leads to irreversible motor neuron damage and paralysis. Endemic wild‐type viral illness has been eradicated in North America as a result of vaccination.
Synonyms
Clinical Presentation
History
VAPP: antecedent administration of OPV from 1 week to 1 month before symptoms; recent administration of DTP (diphtheria, tetanus, pertussis) vaccine may enhance paralysis in active poliovirus infection
Poliomyelitis
Eric J. Sorenson MD, in Neurobiology of Disease, 2007
I. Background
Epidemics of paralytic poliomyelitis occurred regularly before the introduction of the polio vaccination. Such epidemics were most problematic in the developed world. In undeveloped countries, cases were generally sporadic with few epidemics. This difference was largely the result of public health practices in the developed world. In undeveloped countries, polio was transmitted via contaminated drinking water and typically infected infants at a young age. In this young age group, few subjects developed the paralytic form of the disease and most recovered without sequelae but with lifelong immunity. In the developed world with a protected water supply, inoculationoccurred later in life when the probability of the paralytic form of the disease was higher. In addition, without the continuous exposure, conditions were favorable for epidemics.
About half of the patients do not develop paralytic manifestations. In the remaining, a biphasic course evolves. As the initial enteritis subsides, the paralysis begins. Severe back and limb pain, headache, and meningismus develop,
Paralysis tends to occur in a patchy, multifocal distribution.
Recovery depends on collateral sprouting and reinnervation of muscles by surviving motor axons. The paralysis improves over many months to years.
Interactions Between Enteric Viruses and the Gut Microbiota
R.R. Garg, S.M. Karst, in Viral Gastroenteritis, 2016
Poliovirus, a nonenveloped, positive-sense, single-stranded RNA virus, is a member of the Enterovirus genus within the family Picornaviridae.
'PVR transgenic mice are not susceptible to oral poliovirus infection unless they are deficient in the type I interferon (IFN) response (Ohka et al., 2007; Ida-Hosonuma et al., 2005);...'
Providing molecular insight into bacterial enhancement of poliovirus infectivity, N-acetylglucosamine (GlcNAc)-containing polysaccharides expressed on bacterial surfaces including lipopolysaccharide (LPS) and peptidoglycan (PG), also stabilized virus (Kuss et al., 2011; Robinson et al., 2014).
https://www.sciencedirect.com/topics/medicine-and-dentistry/poliomyelitis-virus
https://www.sciencedirect.com/topics/medicine-and-dentistry/poliomyelitis
https://nikiyaantonbettey.blogspot.com/search?q=bioterrorism
Human Immunodeficiency Virus 1
Human immunodeficiency viruses 1 and 2 are retroviruses that exhibit tropism for cells of the immune system with subsequent immune disturbance, especially immunodeficiency.
From: Oh's Intensive Care Manual (Seventh Edition), 2014
Related terms:
AntibodyProteinRNARNA Directed DNA PolymeraseAcquired Immune Deficiency SyndromeHuman Immunodeficiency VirusSimian Immunodeficiency VirusHuman Immunodeficiency Virus 2
Pulmonary Manifestations of Human Immunodeficiency Virus (HIV) Infection
Heather J. Zar, Michael R. Bye, in Pulmonary Manifestations of Pediatric Diseases, 2009
Pathogenesis
HIV-1 is a retrovirus, belonging to a group of heterogeneous, lipid-enveloped RNA viruses. Another retrovirus, HIV-2, is relatively rare and causes a less severe AIDS-like syndrome. HIV-1 has two major viral envelope proteins—the external glycoprotein gp120 and the transmembrane glycoprotein gp41.
The primary target cell of HIV-1 is the human CD4+lymphocyte. The HIV-1 gp120 envelope protein binds to the CD4+ molecule on the host cell membrane with high affinity. This binding allows the virus to enter the T cell and to integrate its genome into the host DNA. HIV-1 also infects monocytesand macrophages but with less marked cytopathic effects. Infected monocytes serve as a reservoir for HIV-1, allowing further spread of the virus throughout the body.5 Infection with HIV-1 results in progressive depletion of the CD4+ helper lymphocytes. This depletion serves as a marker of the severity of HIV-1 infection because the incidence of opportunistic infections and other complications correlates with the number and percentage of CD4+ lymphocytes, particularly in children older than 1 year.6
The ability to produce cytokines, such as interleukin-2 and interferon-γ, is progressively lost in HIV-1-infected children. Natural killer cell–mediated cytotoxicity also is reduced in HIV-1-infected children. In addition, B cell dysfunction with defective humoral immunity further predisposes to severe infection.7
Immunity to Pathogens and Tumors
Stephanie Jost, Marcus Altfeld, in Encyclopedia of Immunobiology, 2016
HIV-1 Escape from NKG2D-Mediated Recognition by NK Cells
HIV-1 infection does not only affect HLA class I expression, thereby impacting recognition by KIRs, but can also trigger the upregulation of ligands for less polymorphic receptors, such as NKG2D. Expression of these stress-induced ligands, and particularly that of UL16-binding proteins (ULBPs), results in increased recognition and killing of both HIV-1-infected and uninfected bystander CD4+ T cells by NK cells (Fogli et al., 2008; Norman et al., 2011; Richard et al., 2013; Ward et al., 2007). Given the high capacity of NKG2D ligands to activate NK cells, HIV-1, like other viruses, has evolved elaborate mechanisms to evade NKG2D-mediated recognition. For instance, the HIV-1 Nef protein appears to not only downregulate HLA-A and HLA-B molecules, but also to limit the expression of NKG2D ligands by triggering the degradation of ULBP-1 and -2, and to a lesser extent, that of MICA (Cerboni et al., 2007). An alternative way for HIV-1 to impair NKG2D-mediated NK cell activation might consist in promoting enzymatic cleavage of MICA and MICB from the surface of HIV-1-infected cells. Engagement of NKG2D by the soluble forms of MICA/B would lead to its downregulation, and to the generation of anergic NK cells. This hypothesis is supported by studies describing elevated plasma levels of soluble MICA and compromised NKG2D-mediated NK cell responses in chronic HIV-1 infection (Nolting et al., 2010), and would explain why MICA has been repeatedly reported to be barely detectable at the surface of CD4+ T cells following HIV-1 infection (Fogli et al., 2008; Ward et al., 2007). Overall, those strategies evolved by HIV-1 to escape from NKG2D recognition suggest that this pathway might play a significant role in the recognition of HIV-1-infected cells by NK cells.
https://www.sciencedirect.com/topics/medicine-and-dentistry/human-immunodeficiency-virus-1
Protozoan Diseases: Malaria Clinical Features, Management, and Prevention
Adrienne J. Showler, ... Andrea K. Boggild, in International Encyclopedia of Public Health (Second Edition), 2017
Malaria and HIV Coinfection
HIV and malaria each negatively affect the outcome and course of the other. HIV-related immune suppression compromises innate host malaria clearance mechanisms, including formation of opsonizing antibodies to Plasmodium. In regions where malaria transmission is low or unstable, HIV-positive adults with malaria are two- to fivefold, which are more likely to have a complicated or severe course. Similarly, HIV coinfection has been demonstrated to be a significant risk factor for severe malaria in areas of stable malaria transmission (Chalwe et al., 2009). HIV-positive children with severe malaria have a threefold higher mortality rate compared with those who are HIV-negative (Hendriksen et al., 2012). HIV has also been shown to impair the response to antimalarial therapy with higher rates of treatment failure among those who are coinfected, in particular, those with low CD4 counts. Malaria upregulates HIV transcription, with coinfected patients demonstrating a transient two- to sevenfold increase in HIV viral load during acute malaria infection. Although this could impact HIV transmission, whether this acute rise in viremia is clinically significant is debatable. However, at least one study in Uganda has shown a significant decline in CD4 counts in HIV-positive patients following episodes of malaria.
https://www.sciencedirect.com/topics/medicine-and-dentistry/human-immunodeficiency-virus
Virus Infections of the Nervous System
Tom Solomon, in Manson's Tropical Infectious Diseases (Twenty-third Edition), 2014
Pathogenesis and Pathology
HTLV-1 is a retrovirus (family Retroviridae; genus Deltavirus) which, like HIV, infects CD4 T cells; after reverse transcription, its DNA becomes incorporated into the DNA of the host cell thus making a provirus. However, whereas HIV eventually destroys the cells it infects, HTLV-1 causes them to proliferate, hence leading to leukaemia in some patients.
Interestingly, HTLV-1 associated myelopathy is more likely when HTLV1 is acquired via blood transfusion, whereas HTLV1 acquired through breast feeding is more likely to be associated with adult T-cell leukaemia-lymphoma. Low levels of viral DNA in peripheral blood mononuclear cells occur in asymptomatic infection while higher levels correlate with symptomatic disease. The host response includes antibody production and development of cytotoxic T cells. These cells, plus CD4 T cells are part of the perivascular inflammatory infiltrate contributing to the myelitis. Neuronal damage is caused by release of inflammatory cytokines, rather than direct viral invasion of neurones.190 Risk factors for development of myelopathyinclude high proviral load and certain polymorphisms in the interleukin (IL)-10 promoter and in the IL28B gene.
HUMAN T-CELL LEUKEMIA VIRUSES (RETROVIRIDAE) | HTLV-2
Bobbie J. Rimel, ... Vicente Planelles, in Encyclopedia of Virology (Second Edition), 1999
Epstein–Barr virus (EBV)-transformed B cell lines have been successfully infected with both HTLV-1 and -2, and HTLV-2 infection results in syncytia formation in the human B cell BJAB lymphoblastoid cell line.
https://www.sciencedirect.com/topics/immunology-and-microbiology/human-t-lymphotropic-virus-1
Human Immunodeficiency Virus 1
Related terms:
Reverse TranscriptaseSimian Immunodeficiency VirusCD4T CellsVaccine EfficacyMonospecific AntibodyMutationHuman Immunodeficiency VirusHuman Immunodeficiency Virus 2
Pulmonary Manifestations of Human Immunodeficiency Virus (HIV) Infection
Heather J. Zar, Michael R. Bye, in Pulmonary Manifestations of Pediatric Diseases, 2009
Pathogenesis
HIV-1 is a retrovirus, belonging to a group of heterogeneous, lipid-enveloped RNA viruses. Another retrovirus, HIV-2, is relatively rare and causes a less severe AIDS-like syndrome. HIV-1 has two major viral envelope proteins—the external glycoprotein gp120 and the transmembrane glycoprotein gp41.
The primary target cell of HIV-1 is the human CD4+lymphocyte. The HIV-1 gp120 envelope protein binds to the CD4+ molecule on the host cell membrane with high affinity. This binding allows the virus to enter the T cell and to integrate its genome into the host DNA. HIV-1 also infects monocytesand macrophages but with less marked cytopathic effects. Infected monocytes serve as a reservoir for HIV-1, allowing further spread of the virus throughout the body.5 Infection with HIV-1 results in progressive depletion of the CD4+ helper lymphocytes. This depletion serves as a marker of the severity of HIV-1 infection because the incidence of opportunistic infections and other complications correlates with the number and percentage of CD4+ lymphocytes, particularly in children older than 1 year.6
The ability to produce cytokines, such as interleukin-2 and interferon-γ, is progressively lost in HIV-1-infected children. Natural killer cell–mediated cytotoxicity also is reduced in HIV-1-infected children. In addition, B cell dysfunction with defective humoral immunity further predisposes to severe infection.7
Immunity to Pathogens and Tumors
Stephanie Jost, Marcus Altfeld, in Encyclopedia of Immunobiology, 2016
HIV-1 Escape from NKG2D-Mediated Recognition by NK Cells
HIV-1 infection does not only affect HLA class I expression, thereby impacting recognition by KIRs, but can also trigger the upregulation of ligands for less polymorphic receptors, such as NKG2D. Expression of these stress-induced ligands, and particularly that of UL16-binding proteins (ULBPs), results in increased recognition and killing of both HIV-1-infected and uninfected bystander CD4+ T cells by NK cells (Fogli et al., 2008; Norman et al., 2011; Richard et al., 2013; Ward et al., 2007). Given the high capacity of NKG2D ligands to activate NK cells, HIV-1, like other viruses, has evolved elaborate mechanisms to evade NKG2D-mediated recognition.
https://www.sciencedirect.com/topics/immunology-and-microbiology/human-immunodeficiency-virus-1
https://www.sciencedirect.com/topics/immunology-and-microbiology/human-t-lymphotropic-virus-1
Immunity to Pathogens and Tumors
Stephanie Jost, Marcus Altfeld, in Encyclopedia of Immunobiology, 2016
HIV-1 Escape from NKG2D-Mediated Recognition by NK Cells
HIV-1 infection does not only affect HLA class I expression, thereby impacting recognition by KIRs, but can also trigger the upregulation of ligands for less polymorphic receptors, such as NKG2D. Expression of these stress-induced ligands, and particularly that of UL16-binding proteins (ULBPs), results in increased recognition and killing of both HIV-1-infected and uninfected bystander CD4+ T cells by NK cells (Fogli et al., 2008; Norman et al., 2011; Richard et al., 2013; Ward et al., 2007). Given the high capacity of NKG2D ligands to activate NK cells, HIV-1, like other viruses, has evolved elaborate mechanisms to evade NKG2D-mediated recognition.
https://www.sciencedirect.com/topics/immunology-and-microbiology/human-immunodeficiency-virus-1
https://www.sciencedirect.com/topics/immunology-and-microbiology/human-t-lymphotropic-virus-1
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