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Medical Microbology
HIV
| Disease | Features |
|---|---|
| Risk Factors for HIV infection | multiple sexual partners; anal sex; traumatic sex; any other STD |
| HIV-1 Causative Agent | human immunodeficiency virus type-1; retrovirus (lentivirus subgroup that infect PMN phagocytes); responsible for AIDS in US and much of the world; enveloped; ssRNA |
| HIV type-2 | structurally similar to HIV-1, except genome is very different; prevalent in West Africa and India; progression to AIDS is slow |
| HIV viral antigens | gp 120, gp 41, p17, p24 |
| gp 120 | SU-surface; glycoprotein; partly responsible for attachment to host cells |
| gp 41 | TM-transmembrane; possible role of entry into host cells |
| p17 | MA-matrix ptn; helps maintain viral structure; transport viral genome to host cell nucleus and assembles new virions |
| p24 | CA-capsid antigen; neucleocapsid (NC); 3 important enzymes (Reverse transciptase (RT), Protease (PR), and Integrase (IN)) along with the 2 ssRNA genome from core of HIV virus |
| gag | Group Antigen gene - translates matrix, capsid and nucleoprotein as a polyprotein which is cleaved by viral protease |
| gag and pol | transcribed as a single unit; translation is often separated |
| PR and RT | targets of major anti-HIV drugs |
| RNA genome of HIV | consists of 9 genes flanked by long terminal repeats (LTRs) |
| gag, pol, and env | genes common to all retroviruses; their protein products are present in virion; functions of genes are very complex and varies depending on cell the type infected |
| HIV Pathogenesis | all cells resond differently; #1 cell type infected is CD4+ Tcells and APCs (both critycal for immune defense against viruses/fungi/some bacteria) |
| CD4 Cell Function | 1. critical for activating macrophages and cytotoxic T lymphocytes, 2. stimultes production of antibodies from B cells |
| HIV - GI epithelium and brain cells | chronic diarrhea, lethargy and dementia |
| HIV attachment to target cell via | host surface CD4 receptor; host must also have coreceptor to ensure viral entry |
| HIV gp120 (SU) | binds host and exposes the binding sites for CD4 receptor and coreceptors |
| Viral penetration into host is mediated by | fusion of grp41 with host cell plasma membrane |
| HIV Variants: Macrophage tropic | interacts with CCR5 on MQ, DC, and CD4 Tcells; responsible for transmission between people |
| HIV Variants: Lymphocyte tropic | interacts with CXCR4 on activated CD4 Tcells |
| Macrophage and DC | first cells to be infected at site of viral entry |
| Macrophage virus switch | to lymphocyte strain in 50% of cases, which starts to infect CD4 Tcells; result = rapid decline of CD4 Tcell count and progression to AIDS |
| Replication of HIV in Host Thelper cells | releases virions from cell lysis |
| Replication of HIV in host macrophages | release of virions occurs over longer period without killing cells |
| HIV is genetically variable due to | high rate of errors during reverse transcription; result is different preferences for host cells, rates of replication, response to host cell immunity... |
| Tcell activation is essential for production of infectious HIV virions with a complete genome | 1. Tcell activation induces low level transcription of provirus; 2. RNA transcripts are spliced to allow synthesis of early ptns Tst and Rev; 3. Tst and Rev go to work; 4. late proteins gag, pol, and env are assembled with genomic RNA into virion buds |
| Tat | (transactivator - positive regulator of transcription); amplifies transcription of viral RNA |
| Rev | (regulator of viral expression - allows export of unspliced and partially spliced transcripts from nuleus); increases transport of singly spliced or unreplicated viral RNA to cytoplasm |
| gag, pol, env | assembled with viral RNA into virions |
| Production of HIV virion from provirus requires | activation of CD4 Tcells; leading to synthesis of transcription factor NFkB |
| NFkB | binds to promoter region of provirus and directs host cell RNA-polymerase to transcribe viral RNA; encodes Tat and Rev ptns |
| Tat binds to transcriptional activation region | (TAR, a sequence in LTR of viral mRNA) to prevent transcription from shutting off |
| Rev ptn controls | supply of viral RNA to cytoplasm and extend of RNA splicing |
| Early in infection, Rev | delivers RNA that encodes ptns needed for making virions |
| Later in infection | viral genomes are supplied, which assembe with viral ptns to form complexes that bud through plasma membrane |
| Mechanisms of Thelper cell destruction | 1. lysis d/t HIV replic; 2. attack of HIV-specific cytotoxic T-cells; 3. NK cell-mediated killing; 4. Ab-dep cell-med cytotoxicity (gp120 on CD4+ SU); 5. autoimmune response; 6. fusion w/infected cells; 7. inc apoptosis; 8. accum of viral ptn in cytoplasm |
| Polyclonal activation of B cells in HIV pts | overwhelms capacity to respond to specific antigens, resulting in unbalanced immune response that can give rise to malignancies or opportunistic infections |
| Depletion of CD4 Tcells | 1. initial drop below 500cells/uL 2. rise in CD4 cells 3. after a variable time, CD4 cells fall for the 2nd time below 500c/uL 4. when CD4 Tcell count <200cells/uL = FULL BLOWN AIDS; often progresses to death |
| Acute Retroviral Syndrome (ARS) | 50-70% of HIV-infected people; 6d-6wk incubation |
| ARS symptoms | sore throat, fever, muscle/headaches, enlarged nodes; rash; disappears w/in a month with attempt to replenish first fall in CD4 count |
| DDx for ARS | flue, infectious mononucleosis |
| ARS asymptomatic period | months -years; virus can be isolated from blood, semen cervix; |
| Long-term non-progresser cases | 5% of HIV-infected/untreated pts show no second decrease in CD4 Tcells after 10yrs |
| Levels of virion in blood: early vs late stage | <10/ml plasma vs 100-1000 |
| Malignant neoplasms and opportunistic infx | when CD4 count <300cell/uL: Kaposi's sarcoma, lymphomas (Bcell; non-hodgkin's; EBV Burkett's), cervical or anal carcinoma |
| Definition of AIDS | HIV+ pts with CD4 Tcell count below 200cells/mL |
| Long-term Non-progressors have mutant CCR5 gene | allows them to remain seropositive for HIV, but maintain a high level of CD4 cells; lack of CCR5 confers resistance to becoming infected with the macrophage-tropic variant |
| CCR5 | a receptor for chemokines CCL3 (MIP-1a), CCL4 (MIP-1b) and CCL5 (RANTES) |
| Mutation of CCR5 | induces a certain degree of immunodeficiency, but with HIV it proves to be an advantage |
| Mutations of CCR5 and Resistance to HIV | mutations must be homozygous; found in 1% of Cauasian population |
| Protozoal Opportunistic Infections in AIDS | toxoplasmosis, isosporal belli infection; cryptosporodiosis |
| Fungal Opportunistic infections in AIDS | pneumocystosis, cryptococcosis, candidiasis, histoplasmosis (disseminated), mycobacterial, disseminated TB (extrapulmonary), mycobacterium avium-intracellulare complex |
| Viral Opportunistic Infections in AIDS | persistant mucocutaneous herpes simplex, cytomegalovirus (retinitis, GI, or disseminated), Varicella zoster (persistent or disseminated), progressive multifocal leukoencephalopathy |
| Dx of AIDS | Early stage - PCR detection of viral RNA/DNA in serum b/c ptns usually non-detectable for 1month; AFTER 1month: viral antibody or components via EIA(ELISA); confirmed by Western blot (envelope ptns gp160, 120, 41, gag, core ptns) |
| Confirming HIV Dx by Western Blot | Positive Sample should exhibit antibodies to both envelope and GAG proteins, or to both envelope proteins (41 and 120/160 kD) |
| HIV Prevention | No vaccine; education about sex and needle exchange; screening blood/organ donors; treating HIV+ moms and babies before and after delivery; avoiding contaminated fluids with delivery (effective c-section or vaginal) |
| Immune response to HIV: Virions | high concentration first 4-8wks, then drops and may rise after 3 years |
| Immune Responses to HIV: Antibodies | Antibodies to HIV envelope ptn and HIV core ptn stay elevated from about 8wks and begin to decline around 2-3 years |
| Immune Response to HIV: HIV-specific cytotoxic Tcells | jump btw 4-8wks and stay pretty high for many years |
| Initial Stages of Immune Response: | 1. Th1 and Th2 responses; 2. production of neutralizing antibodies to envelop/core ptns; 3. generation of cytotoxic CD8 Tcells that kill virus-infected cells |
| Immune response is evaded by mutant strains of HIV: neutralizing antibodies | those generated in initial phase eliminate original strains, but new mutants are selected to survive |
| Immune response is evaded by mutant strains of HIV: Cytotoxic CD8 Tcells | those directed for original HIV strain kill it off, but surivor mutants w/epitope change produce variants |
| Challenges of HIV mutants: | development of anti-HIV vaccine and effective anti-retroviral drugs |
| Basic Mechanisms of HIV Immune Evasion | 1. rapid multiplication (10^10/day); 2. high mutation rate/antigenic variation/immune response cannot keep up with epitopes; 3. elimination of CD4 Tcells by immune mechanisms; 5. Misdirected/exhausted Bcell response |
| Streptococcus pneumoniae immune evasion | capsule; avoids phagocytosis |
| G+ bacteria, some G- bacteria immune evasion | resist insertion of complement MAC; avoids complement-mediated lysis |
| Mycobacterium tuberculosis immune evasion | blocks lysosome fusion with phagosome; avoids antibody and complement opsonization/macrophage killing |
| Listeria monocytogenes immune evasion | escapes phagosome into cytoplasm; avoids macrophage killing and presentation on Class-II MHC |
| Toxoplasma gondii immune evasion | escapes phagosome into own cytoplasmic vesicle; avoids macrophage killing, presentation on both Class-I and Class-II MHC |
| Treponema pallidum immune evasion | covers membrane with host proteins; avoids immune system recognition |
| Herpes virus immune evasion | persist in host cells w/o dividiong (latency); avoid immune system recognition |
| Streptococcus pneumoniae, influenza and HIV immune evasion | antigenic variation; avoids memory response |
| Herpes virus immune evasion | infects cells with little Class-I MHC expression (CNS); avoids presentation on Class-I MHC |
| Staphylococcus aureus, Cytomegalovirus, Herpes simplex virus immune evasion | Expresses membrane Fc-binding protein; Avoids IgG opsonization |
| Neisseria meningitidis, Neisseria gonorrhoeae, Haemophilus influenzae Immune evasion | Expresses IgA protease; Avoids IgA neutralization |
| Herpes simplex virus immune evasion | Expresses membrane complement receptor; Blocks complement function |
| Pseudomonas aeruginosa immune evasion | Secretes elastase that inactivates C3a and C5a; Blocks inflammation |
| Vaccinia virus immune evasion | Expresses complement control protein on infected cell; Blocks complement-mediated lysis of infected cell |
| Vaccinia virus immune evasion | Expresses soluble cytokine receptor; Blocks inflammation |
| Epstein Barr virus (EBV) immune evasion | Inhibits host cell expression of LFA-3, ICAM-1; Blocks adhesion of CTL to infected cells |
| Herpes simplex virus Cytomegalovirus immune evasion | Inhibits host cells Class I expression; Blocks CTL recognition |
| Epstein Barr virus immune evasion | Expresses homolog of IL-10; Inhibits Th1 response, IFNg production, cellular immunity |
| Herpes simplex virus immune evasion | Blocks TAP function; Blocks CTL recognition |
| Staphylococcus aureus immune evasion | Secretes superantigens; Suppresses immune response |
| Hepatitis B Virus, HIV immune evasion | Peptides act as antagonists; T cell activation is blocked |
| Mycobacterium leprae immune evasion | Stimulates Th2 response; Suppresses Th1 response |
| Measles virus immune evasion | Suppresses T and B cell immunity; Suppresses immune response to many pathogens |
| When to initiate HIV treatment? | As soon as infx is detected (CD4 count <500 or plasma HIV viral RNA load >5000) |
| Determinants against starting HIV treatment | drug toxicity, resistance development, quality of life, cost, patient compliance |
| Death rate from HIV since 1998 | declined d/t early Dx and Tx with HAART |
| HAART (highly active antiretroviral therapy) | coctail of reverse transcriptase and protease inhibitors, once a day therapy; does NOT cure AIDS, rather it controls viremia and increases CD4 counts |
| Nucleoside reverse transcriptase inhibitors (NRTI) | AZT, D4T, 3TC, ddl, ddC |
| Non-nucleoside reverse transcriptase inhibitors | nevirapine, delavirdine, efavirenz |
| HIV Protease Inhibitors | prevent packaging of viral proteins into virion; Saquinavir, ritonavir, indinavir, nelfinavir |
| NTRI Mode of Action | similar to purine/pyrimidine viral nucleic acids --> incorporates into growing viral DNA chain during replication to block completion |
| In addition to primary HIV treatment, prophylaxis against opportunistic infx is given | when CD4 count <200 - P. carinii; when CD4 count <75 - mycobacterial and fungal infx |
| Resistance HIV Treatment | protease inhibitors - one mutation for resistance can occur w/in days; RTIs - 3 to 4 independent mutations over months |
| Retroviral Transformation facilitates oncogenesis | continual replication w/o cell death; integration of a DNA copy of viral RNA into host genome |
| 3 mechanisms of retroviral transformation | 1. oncogens - loss of normal growth control; 2, insertional mutagenesis (insertion of provirus into DNA next to proto-oncogene); 3. expression of trans gene that transcriptionally activates other cellular genes that allows cell proliferation |
| Kaposi's Sarcoma | tumor arising from blood or lymph vessels (other forms in older men of eastern europe/africa/mediterranean; w/ AIDS associated herpesvirus-8 (HHV-8) |
| Kaposi's Sarcoma and HHV-8 | infection w/HIV-1 and HHV-8 greater risk of cancer; mostly latent; cells become lytic and lead to changes causing tumors -- 1. cells become spindly and proliferate; 2. extensive angiogenesis; |
| Connection btw HIV-1, HHV-8 and Kaposi's | HIV-1 induced Tat causes endothelial proliferation and the co-infection with HHV-8 favors malignant transformation |
| Lymphoma and AIDS | 1st HIV case was isolated from a pt w/lymphadenopathy; proliferation d/t disregulated cytokine production compensating for lymphoic cell death in HIV and in response to viral gp41 antigen; B-cell lymphomas more common than T; |
| Epstein-Barr virus (EBV), Lymphoma, AIDS | Probably EBV indirectly causes B-cell lymphoma in AIDS; especially in brain and Burkett's lymphoma is 1000x for frequent; |
| EBV and HIV Mechanism of Action | latent EBV by HIV infection; EBV infects new Bcells with polyclonal proliferation and inc lifespan; malignant Bcells though to arise from this population of rapidly dividing cells |
| HPV, Cervical and Anal carcinoma and AIDS | HPV-16/18 ONLY; sexual transmission infects cervical/anal epithelium; viral product blocks cell cycle regulators; HPV replication increases with decreased host cellular immunity; AIDS pts should be screened biannually |
| Toxoplasmosis gondii - causative agent | obligate intracellular sporozoan; reproduces in GI of cats; oocytes passed in feces; morphology - oocyst, trophozoite, tissue cyst |
| T. gondii in humans | brain, heart, skeletal muscle tissue cysts form from trophozoites and their protective membrane |
| T. gondii epidemiology | worldwide, but >in tropics; 50% US pop seropositive |
| T. gondii transmission | 1. ingestion of oocysts (kids playing in litter box); 2. ingestion of tissue cyst in meat; 3. congenital 1/500 births; 4. transfusion/organ transplant |
| Congenital toxoplasmosis - severe | abortion or stillbirth; live born w/CNS and visceral probs: micro/hydrocephaly, cerebral calcifications, convulsions, psychomotor retardation; hepatitis, pneumonia |
| congenital toxoplasmosis - mild form | infected in 3rd trimester; healthy at birth w/later onset of epilepsy, MR, strabismus; very delayed Chorioretinitis - eye pain/loss of acuity from reactivation of latent infx in 20s |
| Toxoplasmosis - Normal Hosts | asymptomatic localized lymphadenopathy (cervical); fever, sore throat, rash, hepatosplenomegaly (mimicks mono); ALSO occasionally, severe visceral meningoencephalitis, pneumonitis, myocarditis, hepatitis |
| Toxoplasmosis - Immunocompromised hosts | reaction from latent infection; 50% of AIDS pts form Toxoplasmic encephalitis w/90% fatal |
| Toxoplasmosis Diagnosis | detection of IgG via indirect hemagglutination or indirect fluorescence OR demonstration of trophozoites in lymph node w/Wright or Giemsa stain |
| Toxoplasmosis Prevention | handwashing after handling uncooked meat; properly cook/freeze meat; avoid cat feces; prevent cats from hunting or eating raw meat |
| Toxoplasmosis Treatment | pyrimentamine and sulfonamides (not against cyst form); pregnancy - spiramycin (cytostatic macrolide); CYST and TROPHOXOITE - atovaquone used in radical cure of toxoplasma encephalitis |
| Cryptosporidium Gastroenteritis | obligate intracelular sporozoan parasite; C.paryum - spherical attach to epithelial microvilli, stains with Giemsa and HE; oocysts are acid fast |
| Cryptosporidiosis Epidemiology | animal reservoir and person-person transmition; water contamination in cities; kids at most risk, followed by immunodeficient/AIDS pts |
| Cryptosporidiosis Pathogenesis | entire GI tract, esp jejunum; villous atrophy, crypt enlragment and MNC in lamina propria |
| Cryptosporidiosis Symptoms - Normal Pts | abdominal pain and profuse, watery diarrhea 5-10days, nausea, anorexia, vomiting, low fever, complete recovery w/o reinfx or relapse |
| Cryptosporidiosis Symptoms - Immunocompromised Pts | (childhood malnutrition, AIDS, congenital hypogammaglobulinemia, cancer chemotherapy, transplant pts); indolent onset; severe diarrhea and other "normal" symptoms, but CHRONIC illness unless immune status is improved |
| Cryptosporidiosis Dx | ID oocysts in stool via acid-fast or immunofluorescent Ab (ELISA) |
| Cryptosporidiosis Prevention and Tx | stool precautions; rehydration, supportive Tx; if drug-induced immunosuppression stop Rx; NO Drugs available |
| Mycobacterium avium-intracellulare complex | a group of acid-fast organisms that can be divided into serotypes; second to M. tuberculosis as cause of disease in US; resistant to antitubercular drugs; may require surgery |
| M. avium-intracellular complex - manifestations | Most common systemic bacterial infx in AIDS pts; cavity pulmonary disease (superimposed on chronic lung disease), cervical lymphadenitis, osteomyelitis, renal and skin infection |
| M. avium-intracellulare complex - symptoms, Dx, prognosis | progressive weight loss, intermittent fever, chills, night sweats, diarrhea; blood culture/DNA probes; grave |
| Mycobacterium kansasii infection | 3% of mycobacterial diseases in US (cities, IL, OK, TX); photochromogenic - yellow colonies |
| M. kansasii - symptoms, Dx, Tx | TB-like symptoms (cavity pulmonary disease, cervical lympadenitis, skin infx; disseminated in AIDS pts); PPD+; Rx - INH, rifampin, ethambutol |
| nef | negative regulation factor - augments viral replication in vivo and in vitro; downregulates CD4 and MCH Class-II |
| Pneumocystis carinii pneumonia (Pneumocystosis) | d/t Pneumocystis carinii "fungus" that lacks ergosterol in cell wall and is not sensitive to traditional antifungal drugs; spread in infants/elderly/immunocompromised thru air (latent or new infx) |
| Pneumocystosis symptoms | gradual onset, SOB/rapid, low-grade fever, 50% have non-productive cough, dusky skin/mucous membranes d/t poor oxygenation in advanced stages...DEATH from respiratory failure |
| Pneumocystosis pathoghenesis | inhalation of P. carinii spores, attachement to alveolar walls, inflammatory response w/MNC and fluid accumulation in alveoli w/multiplying fungi; Later = thickened/scarred alveolar walls that prevent passage of O2 |
| X-ray findings in Pneumocystis pneumonia | Interstitial pneumonia in an AIDS pt has linear opacities w/hazy ground glass appearance |
| Pneumocystosis diagnosis | NOT sputum b/c it's deeper than bronchi; BRONCHOALVEOLAR LAVAGE is least invasive (needle aspiration, biopsy, etc); cysts or trophozites by Wright, Giemsa, Papanicolaou stains; Confirm w/methanamine or antibody (PCR in future) |
| Pneumocystosis Prevention and Treatment | 2nd largest cause of death in AIDS pts; rates lowered w/use of Trimethoprim-sulphamethoxazole (TSX) when CD4<200 in addition to anti-HIV drug regimen |
| Pneumocystosis Immunity | cell-mediated (macrophages and CD4 lymphocytes) play biggest protective role against P. carinii; Antibodies against surface glycoprotein and other antigens also play roles |
| Cryptococcus neoformans | C. neoformans is yeast w/thick capsule (polysaccharide polymer - GXM) that does not stain w/indian ink; grows at 35-37* on blood, chocolate, sabouraud and potato dextrose agars in 1-2 days resembles bacterial colonies |
| Cryptococcus neoformans epidemiology | soils contaminated with guano (bird droppings); sporadic, no occupational predisposition; CD4-compromised pts are susceptible (one of the top 4 killers in AIDS) |
| Crytococcus neoformans Pathogenesis | yeast makes antiphagocytic capsule in respiratory tract (Virulence factor: interferes w/antigen presentation cell-mediated response and downreg of WBC migration); disseminates to CNS (meningoencephalitis); Melanin protects from oxid injury; rxn varies |
| Cryptococcus neoformans symptoms | Most common presentation: Meningitis (slow, headache/dizzy; impaired cerebral fxn, fever, seizures, CN signs, dementia, LOC); rapidly worsens w/AIDS (5-15% of AIDS pts); Pneumonia is ASYMPTOMATIC |
| Cryptococcus neoformans diagnosis | CSF: inc pressure, pleocytosis (>100 cells w/mostly lymphocytes; dec glucose); Isolate C. neoformans from centrifuged CSF sediments/stain w/indian ink; Detect GXM polysac antigen in CSF or serum (latex agglutination or enzyme immunoassay) |
| Cryptococcus neoformans treatment | Amphoterecin B in combo w/Flucytosine or Fluconazole; 75% of pts respond to Tx, but relapse; chronic = repeated Tx; 50% of cured have residual damage |
| Cyclomegalovirus disease agent | largest member of Herpesviridae family; enveloped dsDNA; infected cells double in size; usually a latent infx that reactivates later; may be a lytic infxn; Intranuclear inclusion bodies make a "owl's eye appearance |
| Cytomegalovirus epidemiology | 50% of pop is seropositive; transmitted by contact/sexual/transfusion/transplant/pregnancy; risk at day care; isolated from urine/saliva/semen/cervical secretions; infxn is lifelong (latent in leukocytes) |
| Cytomegalovirus pathogenesis | infects: eye, CNS, liver tissue; can be latent or active; replication depends on infected cell type (monocytes:low vs. lymphocytes:latent); immunosuppression activates cycle; CMV inhibits MHC transfer to surface of infected cells to evade immune response |
| Cytomegalovirus manifestations: Congenital cytomegalic inclusion disease | jaundice, hepatomegaly, anemia, chorioretinitis, low birth wt, microcephaly; remain asymptomatic for years w/5-25% hearing loss, MR, etc later |
| Cytomegalovirus manifestations: Acute infections in immunocompetent hosts | asymptomatic, but teens/YAs can develop infectious mononucleosis-like symptoms (fever, fatigue, splenomegaly, lymphadenopathy) |
| Cytomegalovirus manifestations: immunocompromised pts | Suffer from the severe form of the disease (pneumonia, chorioretinitis, gastroenteritis, neurologic disorders) |
| Cytomegalovirus diagnosis | detection of CMV cytopathology, antigen or DNA in infected tissue; Isolateing virus from tissue or secretions; Demonstrating seroconversion (presence of specific IgM antibody) |
| Cytomegalovirus prevention | (vaccine in clinical trials); screen blood/organ donors; safe sex; hyperimmune human anti-CMV globulin for CMV pneumonia in transplant recipients |
| Cytomegalovirus treatment | Gancyclovir (inhibits DNA polymerase, bone marrow suppression); Foscarnet (inhibits DNA pol, nephrotoxic); Cidofovir (nucleotide agent, nephrotoxic) for retinitis; *Gancyclovir + immune globulin is effective in dec high mortality of CMV pneumonia* |
| HIV compatible vaccines | MMR, pneumococcal polysaccharide, influenza, HAV, HBV |
| HIV non-compatible vaccines | oral poliomyelitis, oral typhoid, BCG (TB vaccine), varicella-zoster, yellow fever |
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