Mollicutes at the US National Library of Medicine Medical Subject Headings (MeSH)
https://en.wikipedia.org/wiki/Mollicutes
https://en.wikipedia.org/wiki/Methotrexate
https://en.wikipedia.org/wiki/Treponema_pallidum
https://en.wikipedia.org/wiki/Myxococcus
https://en.wikipedia.org/wiki/Phagemid
https://en.wikipedia.org/wiki/Bacillus_subtilis
https://en.wikipedia.org/wiki/Gammaretrovirus
https://en.wikipedia.org/wiki/Woolly_monkey_sarcoma_virus
https://en.wikipedia.org/wiki/Reticuloendotheliosis_virus
https://en.wikipedia.org/wiki/Chick_syncytial_virus
https://en.wikipedia.org/wiki/Gammaretrovirus
https://en.wikipedia.org/wiki/Spumaretrovirinae
https://en.wikipedia.org/wiki/Progressive_vaccinia
https://en.wikipedia.org/wiki/Generalized_vaccinia
https://en.wikipedia.org/wiki/Vaccinia
https://en.wikipedia.org/wiki/Palmoplantar_keratoderma
https://en.wikipedia.org/wiki/Dystrophic_calcification
https://en.wikipedia.org/wiki/Calciphylaxis
https://en.wikipedia.org/wiki/NF-κB
https://en.wikipedia.org/wiki/Endogenous_retrovirus#Human_endogenous_retroviruses
https://en.wikipedia.org/wiki/Gammaretrovirus
https://en.wikipedia.org/wiki/Spumaretrovirinae
https://en.wikipedia.org/wiki/Bovine_leukemia_virus
https://en.wikipedia.org/wiki/Phagemid
https://en.wikipedia.org/wiki/Mycoplasmataceae
https://en.wikipedia.org/wiki/Mycobacterium_tuberculosis
https://en.wikipedia.org/wiki/Caseous_necrosis
https://en.wikipedia.org/wiki/Necrosis
https://en.wikipedia.org/wiki/Gas_gangrene
https://en.wikipedia.org/wiki/Syphilis
https://en.wikipedia.org/wiki/HIV
https://en.wikipedia.org/wiki/Pyroptosis
https://en.wikipedia.org/wiki/Immunosuppressive_drug
https://en.wikipedia.org/wiki/Human_foamy_virus
https://en.wikipedia.org/wiki/House_dust_mite
https://en.wikipedia.org/wiki/Crustacean
https://en.wikipedia.org/wiki/Parasitism
https://en.wikipedia.org/wiki/Neurosarcoidosis
https://en.wikipedia.org/wiki/Timeline_of_human_vaccines
https://en.wikipedia.org/wiki/Neurocysticercosis
https://en.wikipedia.org/wiki/Smallpox
https://en.wikipedia.org/wiki/Measles
https://en.wikipedia.org/wiki/Malaria
https://microbewiki.kenyon.edu/index.php/Granulosis_Virus
https://en.wikipedia.org/wiki/Rabies
https://en.wikipedia.org/wiki/Ricketts
https://en.wikipedia.org/wiki/Leishmania
https://en.wikipedia.org/wiki/Granulation
https://en.wikipedia.org/wiki/Allergy
https://en.wikipedia.org/wiki/Rhinitis
https://en.wikipedia.org/wiki/Rash
https://en.wikipedia.org/wiki/Chickenpox
https://en.wikipedia.org/wiki/Eczema_vaccinatum
https://en.wikipedia.org/wiki/Lupus_erythematosus
https://en.wikipedia.org/wiki/Chromosome_21
https://en.wikipedia.org/wiki/Calciphylaxis
https://en.wikipedia.org/wiki/Dystrophic_calcification
https://en.wikipedia.org/wiki/NF-κB
https://en.wikipedia.org/wiki/Endogenous_retrovirus#Human_endogenous_retroviruses
https://en.wikipedia.org/wiki/Gammaretrovirus
https://en.wikipedia.org/wiki/NK-92
https://en.wikipedia.org/wiki/Rhizomucor_pusillus
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus_1
https://en.wikipedia.org/wiki/Feline_leukemia_virus
https://en.wikipedia.org/wiki/Tumor_lysis_syndrome
https://en.wikipedia.org/wiki/Tumor_necrosis_factor
https://en.wikipedia.org/wiki/Rhabdomyolysis
https://en.wikipedia.org/wiki/Caprine_arthritis_encephalitis_virus
https://en.wikipedia.org/wiki/Jaagsiekte_sheep_retrovirus
https://en.wikipedia.org/wiki/Visna-maedi_virus
https://en.wikipedia.org/wiki/Bacillus_thuringiensis
https://en.wikipedia.org/wiki/Lentivirus
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus
https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus
https://en.wikipedia.org/wiki/Treponema_pallidum
https://seer.cancer.gov/seertools/hemelymph/51f6cf57e3e27c3994bd5363/?q=cytoid#
https://seer.cancer.gov/seertools/hemelymph/532b32a0e4b0626b1926e990/
https://en.wikipedia.org/wiki/Myxococcus
https://en.wikipedia.org/wiki/Methotrexate
https://en.wikipedia.org/wiki/Pseudomonas_aeruginosa
https://en.wikipedia.org/wiki/Leukemia
https://en.wikipedia.org/wiki/Provirus
https://en.wikipedia.org/wiki/Bacillus_coagulans
https://en.wikipedia.org/wiki/Monckeberg%27s_arteriosclerosis
https://en.wikipedia.org/wiki/NF-κB
https://en.wikipedia.org/wiki/Dystrophic_calcification
https://en.wikipedia.org/wiki/Generalized_vaccinia
https://en.wikipedia.org/wiki/Progressive_vaccinia
https://en.wikipedia.org/wiki/Wart
https://en.wikipedia.org/wiki/Eczema_vaccinatum
https://en.wikipedia.org/wiki/Category:Bacteria_described_in_1915
https://en.wikipedia.org/wiki/Calciphylaxis
https://en.wikipedia.org/wiki/NF-κB
https://en.wikipedia.org/wiki/Dystrophic_calcification
https://en.wikipedia.org/wiki/Human_foamy_virus
https://en.wikipedia.org/wiki/Avian_sarcoma_leukosis_virus
https://en.wikipedia.org/wiki/Allergic_rhinitis
https://en.wikipedia.org/wiki/Bacillus_subtilis
https://en.wikipedia.org/wiki/Bacillus_atrophaeus
https://en.wikipedia.org/wiki/Rotavirus
https://en.wikipedia.org/wiki/Shigellosis
https://en.wikipedia.org/wiki/Pollen
https://en.wikipedia.org/wiki/Microsporangia
https://en.wikipedia.org/wiki/Common_cold
https://en.wikipedia.org/wiki/Bacillus_subtilis
https://en.wikipedia.org/wiki/Bacillus_atrophaeus
https://en.wikipedia.org/wiki/Radiotrophic_fungus
https://en.wikipedia.org/wiki/Psammophile
https://en.wikipedia.org/wiki/Psychrophile
https://en.wikipedia.org/wiki/Piezophile
https://en.wikipedia.org/wiki/Osmophile
https://en.wikipedia.org/wiki/Lipophilic_bacteria
https://en.wikipedia.org/wiki/Cytokinesis
https://en.wikipedia.org/wiki/Cytokine
https://en.wikipedia.org/wiki/Methylation
https://en.wikipedia.org/wiki/Category:Epigenetics
https://en.wikipedia.org/wiki/Epigenetic_clock
https://en.wikipedia.org/wiki/Category:Papillomavirus-associated_diseases
https://en.wikipedia.org/wiki/Molluscum_contagiosum_virus (Petersen & Smith; USA; NAC)
https://en.wikipedia.org/wiki/Basal-cell_carcinoma
https://en.wikipedia.org/wiki/Herpesviridae
NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.[2][3][4][6][7] NF-κB plays a key role in regulating the immune response to infection. Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development. NF-κB has also been implicated in processes of synaptic plasticity and memory.[8][9][10][11][12][13]
https://en.wikipedia.org/wiki/NF-κB
Human parainfluenza viruses (HPIVs) are the viruses that cause human parainfluenza. HPIVs are a paraphyletic group of four distinct single-stranded RNA viruses belonging to the Paramyxoviridae family. These viruses are closely associated with both human and veterinary disease.[2] Virions are approximately 150–250 nm in size and contain negative sense RNA with a genome encompassing about 15,000 nucleotides.[3]
The viruses can be detected via cell culture, immunofluorescent microscopy, and PCR.[4] HPIVs remain the second main cause of hospitalisation in children under 5 years of age suffering from a respiratory illness (only Human orthopneumovirus, or Respiratory syncytial virus (RSV), causes more respiratory hospitalisations for this age group).[5]
https://en.wikipedia.org/wiki/Human_parainfluenza_viruses
The first HPIV was discovered in the late 1950s. The taxonomic division is broadly based on antigenic and genetic characteristics, forming four major serotypes or clades, which today are considered distinct viruses.[6]These include:
| Virus | GenBank acronym | NCBI taxonomy | Notes |
|---|---|---|---|
| Human parainfluenza virus type 1 | HPIV-1 | 12730 | Most common cause of croup |
| Human parainfluenza virus type 2 | HPIV-2 | 11212 | Causes croup and other upper and lower respiratory tract illnesses |
| Human parainfluenza virus type 3 | HPIV-3 | 11216 | Associated with bronchiolitis and pneumonia |
| Human parainfluenza virus type 4 | HPIV-4 | 11203 | Includes subtypes 4a and 4b |
HPIVs belong to two genera: Respirovirus (HPIV-1 & HPIV-3) and Rubulavirus (HPIV-2 & HPIV-4).[3]
https://en.wikipedia.org/wiki/Human_parainfluenza_viruses
Pneumoviridae (from Greek pneumo-, lung, -viridae, virus from Latin, poison, slimy liquid)[2][3] is a family of negative-strand RNA viruses in the order Mononegavirales.[1][4] Humans, cattle, and rodents serve as natural hosts.[5] Respiratory tract infections are associated with member viruses such as human respiratory syncytial virus. There are five species in the family which are divided between the genera Metapneumovirus and Orthopneumovirus. The family used to be considered as a sub-family of Paramyxoviridae, but has been reclassified as of 2016.[1]
| Genus | Species | Virus (Abbreviation) |
| Metapneumovirus | Avian metapneumovirus | avian metapneumovirus (AMPV) |
| Human metapneumovirus | human metapneumovirus (HMPV) | |
| Orthopneumovirus | Bovine orthopneumovirus | bovine respiratory syncytial virus (BRSV) |
| Human orthopneumovirus | human respiratory syncytial virus A2 (HRSV-A2) | |
| human respiratory syncytial virus B1 (HRSV-B1) | ||
| Murine orthopneumovirus | murine pneumonia virus (MPV) |
https://en.wikipedia.org/wiki/Pneumoviridae
https://en.wikipedia.org/wiki/Crimean–Congo_hemorrhagic_fever
Thogotovirus is a genus of enveloped RNA viruses, one of seven genera in the virus family Orthomyxoviridae. Their single-stranded, negative-sense RNA genome has six or seven segments. Thogotoviruses are distinguished from most other orthomyxoviruses[3] by being arboviruses – viruses that are transmitted by arthropods, in this case usually ticks. Thogotoviruses can replicate in both tick cells and vertebrate cells; one subtype has also been isolated from mosquitoes. A consequence of being transmitted by blood-sucking vectors is that the virus must spread systemically in the vertebrate host – unlike influenza viruses, which are transmitted by respiratory droplets and are usually confined to the respiratory system.[4]
The genus contains the species Thogoto thogotovirus and Dhori virus (DHOV), and the latter's subtype Batken virus, as well as the species or strains Araguari virus, Aransas Bay virus (ABV), Bourbon virus, Jos virus (JOSV) and Upolu virus (UPOV), which have yet to be confirmed by the International Committee on Taxonomy of Viruses (ICTV). A wide range of mammals are infected by members of the genus; some types also infect birds. THOV causes disease in livestock. THOV, DHOV and Bourbon virus can infect humans, and have occasionally been associated with human disease.
https://en.wikipedia.org/wiki/Thogotovirus
Arbovirus is an informal name for any virus that is transmitted by arthropod vectors. The term arbovirus is a portmanteau word (arthropod-borne virus).[1] Tibovirus (tick-borne virus) is sometimes used to more specifically describe viruses transmitted by ticks, a superorder within the arthropods.[2] Arboviruses can affect both animals (including humans) and plants. In humans, symptoms of arbovirus infection generally occur 3–15 days after exposure to the virus and last three or four days. The most common clinical features of infection are fever, headache, and malaise, but encephalitis and viral hemorrhagic fever may also occur.[3]
https://en.wikipedia.org/wiki/Arbovirus
Viral hemorrhagic fevers (VHFs) are a diverse group of animal and human illnesses in which fever and hemorrhage are caused by a viral infection. VHFs may be caused by five distinct families of RNA viruses: the families Filoviridae, Flaviviridae, Rhabdoviridae, and several member families of the Bunyavirales order such as Arenaviridae, and Hantaviridae. All types of VHF are characterized by fever and bleeding disorders and all can progress to high fever, shock and death in many cases. Some of the VHF agents cause relatively mild illnesses, such as the Scandinavian nephropathia epidemica (a hantavirus), while others, such as Ebola virus, can cause severe, life-threatening disease.
https://en.wikipedia.org/wiki/Viral_hemorrhagic_fever
The human immunodeficiency viruses (HIV) are two species of Lentivirus (a subgroup of retrovirus) that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS),[1][2] a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive.[3] Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[4] In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids. Research has shown (for both same-sex and opposite-sex couples) that HIV is untransmittable through condomless sexual intercourse if the HIV-positive partner has a consistently undetectable viral load.[5][6] Non-sexual transmission can occur from an infected mother to her infant during pregnancy, during childbirth by exposure to her blood or vaginal fluid, and through breast milk.[7][8][9][10] Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.
HIV infects vital cells in the human immune system, such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[11] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[12] apoptosis of uninfected bystander cells,[13]direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8+ cytotoxic lymphocytes that recognize infected cells.[14] When CD4+ T cell numbers decline below a critical level, cell-mediated immunityis lost, and the body becomes progressively more susceptible to opportunistic infections, leading to the development of AIDS.
https://en.wikipedia.org/wiki/HIV
COVID VACCINE ANTICIPATION CONSIDERATIONS EXEPT THEFT OF CELL, SEQUENCE, CODE, TECHNOLOGY, INTELLECTUAL PROPERTY, ETC..
Erythropoietic protoporphyria (or commonly called EPP) is a form of porphyria, which varies in severity and can be very painful. It arises from a deficiency in the enzyme ferrochelatase, leading to abnormally high levels of protoporphyrin in the red blood cells (erythrocytes), plasma, skin, and liver.[2] The severity varies significantly from individual to individual.
A clinically similar form of porphyria, known as X-Linked dominant protoporphyria, was identified in 2008.[3]
Haematin (also known as hematin, ferriheme, hematosin, hydroxyhemin, oxyheme, phenodin, or oxyhemochromogen) is a dark bluish or brownish pigment containing iron in the ferric state, obtained by the oxidation of haem.[1]
Haematin inhibits the synthesis of porphyrin, and stimulates the synthesis of globin. It is a component of cytochromes and peroxidases, and is also used as a reagent.[2]
https://en.wikipedia.org/wiki/Haematin
The globins are a superfamily of heme-containing globular proteins, involved in binding and/or transporting oxygen. These proteins all incorporate the globin fold, a series of eight alpha helical segments. Two prominent members include myoglobin and hemoglobin. Both of these proteins reversibly bind oxygen via a heme prosthetic group. They are widely distributed in many organisms.[2]
https://en.wikipedia.org/wiki/Globin
https://en.wikipedia.org/wiki/Globulin
https://en.wikipedia.org/wiki/Globular_protein
Crohn's resistance was a result of the absence of a receptor, which prevent the HIV from infecting CD4 present on the exterior of the white blood cells. The absence of such receptors, or rather the shortening of them to the point of being inoperable, is known as the delta 32 mutation.[4] This mutation is linked to groups of people that have been exposed to HIV but remain uninfected such as some offspring of HIV positive mothers, health officials, and sex workers.[5]
C-C chemokine receptor type 5, also known as CCR5 or CD195, is a protein on the surface of white blood cells that is involved in the immune system as it acts as a receptor for chemokines. This is the process by which T cells are attracted to specific tissue and organ targets. Many strains of HIV use CCR5 as a co-receptor to enter and infect host cells. A few individuals carry a mutation known as CCR5-Δ32 in the CCR5 gene, protecting them against these strains of HIV.[citation needed]
In humans, the CCR5 gene that encodes the CCR5 protein is located on the short (p) arm at position 21 on chromosome 3. A cohort study, from June 1981 to October 2016, looked into the correlation between the delta 32 deletion and HIV resistance, and found that homozygous carriers of the delta 32 mutation are resistant to M-tropic strains of HIV-1 infection.[9] Certain populations have inherited the Delta 32 mutation resulting in the genetic deletion of a portion of the CCR5 gene.[10][excessive citations]
In 2019, it was discovered that the mutation of TNPO3 that is the cause of type 1F limb-girdle muscular dystrophy (LGMD1F), also causes innate resistance to HIV-1.[11] The gene TNP03 was known to be involved into virus transportation into the infected cells. Blood samples from a family affected by LGMD1F showed a resistance to HIV infection. While the CCR5Δ32 deletion blocks the entry of virus strains that use the CCR5 receptor, the TNPO3 mutation causing LGMD1F blocks the CXCR4 receptor, making it effective on different HIV-1 strains, due to HIV tropism.[citation needed]
Cytotoxic T-lymphocytes (CTLs) provide a protective reaction against HIV when consistent exposure to the virus is present. Sex workers are found to have these CTLs within genital mucus, preventing the spread of HIV within heterosexual transmission. While creating a protective seal, CTLs become ineffective when lapses in HIV exposure occur, which leads to the possibility of CTLs only being an indicator of other genetic resistances towards HIV, such as immunoglobulin A responses within vaginal fluids.[5][12]
Chimpanzees in African countries have been found to develop AIDS at a slower rate than humans. This resistance is not due to the primate's ability to control the virus in a manner that is substantially more effective than humans, but rather because of the lack of tissues created within the body that typically progress HIV to AIDS. The chimpanzees also lack CD4 T cells and immune activation that is required for the spread of HIV.[12]
Another method used by the Kiem lab was the release of zinc finger nuclease (ZFN), which identifies specific sections of DNA to cause a break in the double helix. These ZFNs were used to target CCR5 in order to delete the protein, halting the course of the infection.[13]
While the delta mutation has been observed to prevent HIV in specific populations, it has shown little to no effect between healthy individuals and those who are infected with HIV among Iranian populations. This is attributed to individuals being heterozygous for the mutation, which prevents the delta mutation from effectively prohibiting HIV from entering immune cells.[15]
https://en.wikipedia.org/wiki/Innate_resistance_to_HIV
With in vitro transcription techniques three suggested ORFs on chromosome 3 (gag), 6 (pro) and 7 (env) were detected and further analyzed revealing that the ORF on chromosome 7q21.2 uniquely encoded a glycosylated Env protein.[12] Performing RealTime RT-PCR on adrenal gland, bone marrow, cerebellum, whole brain, fetal brain, fetal liver, heart, kidney, liver, lung, placenta, prostate, salivary gland, skeletal muscle, spinal cord, testis, thymus, thyroid gland, trachea, and uterus cells revealed 22 complete HERV-W families on chromosomes 1–3, 5–8, 10–12, 15, 19 and X.[6]
In silico expression data revealed that these HERV-W elements are randomly expressed in various tissues (brain, mammary gland, cerebrum, skin, testis, eye, embroyonic tissue, pancreatic islet, pineal gland, endocrine, retina, adipose tissue, placenta and muscle).[6]
Further, human tissues that lack some sort of HERV expression could not be found which suggests that HERVs are permanent members of the human transcriptome.[13] Although expression of HERV-W is prevalent in the whole body there are two tissues whose expression levels are higher than the rest. The HERV-W derived element of chromosome 12p11.21 and 7q21.2 had 42 hits from the env gene in pancreatic islet tissues and 224 hits (11 gag, 41 pol, 164 env) in placenta, testis, and embryotic tissues, respectively. The HERV-W element on 7q21.2 encodes for ERVWE-1, which was named synctin-1.[14]
As a control a gene known to be hyperfusogenic, A-Rless, was transfected into the cell-line . Upon transfection of cells with this vector there was only a 6% fusion of cells as opposed to a 48% fusion with the HERV-W vector, thus revealing the gene encoded by HERV-W env is a highly fusogenic membrane glycoprotein.[15]
Furthermore, HERV-W env glycoprotein has been shown to contain an immunosuppressive region.[21] This immunosuppressive nature of synctin-1 and/or synctin-2 (HERV-W) may be key in creating an immunologic barrier between the mother and the fetus.[22] Since the fetus only share half of the mother's DNA it is critical that the mother's immune system does not reject or attack the fetus.[23]
https://en.wikipedia.org/wiki/Human_Endogenous_Retrovirus-W
However, using a luciferase reporter gene assay HERV-Ws that have incomplete LTR's were still found to have promoter activity. This suggests that the transcription of HERV's can be activated not just by LTR- directed transcription but also by transcriptional leakage.[25] Meaning if a nearby gene is being transcribed the transcription factors and polymerase can just keep moving along the DNA reaching the nearby HERV, where they can then transcribe it. In fact by doing a Chip-seq analysis of HERV-W LTR's it was found that ¼ of HERV-W LTR's can be bound by transcription factor p56 (ENCODE Project). This indicates a reason behind HERV-W's cell specific expression.
https://en.wikipedia.org/wiki/Human_Endogenous_Retrovirus-W
| Mucolipidosis type IV | 1:90 to 1:100 in Ashkenazi Jews | MCOLN1 PetersenSmithUSAMisterGenModCloHybrJJ |
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