 system, cells of the intestine and bone marrow cells. The victim typically dies two to ten years after the initial asymptomatic period, following a protracted and painful illness.
Human immunodeficiency virus, a retrovirus, is the etiological agent of AIDS, as well as of a variety of related disorders, such as AIDS Related Complex (ARC). HIV infection begins when a virion or virus-infected cell binds to susceptible cells and fuses with them, injecting the core protein and viral RNA into the cell. The RNA is transcribed to viral DNA. The double stranded DNA migrates to the nucleus and is integrated into the cell's DNA. The viral DNA can remain dormant for an indefinite period of time, or the genes can replicate and be translated into viral proteins. The viral proteins are assembled into new virions that bud from the cell, spreading the disease.
HIV preferentially infects the T4 lymphocytes, immune cells important in helping to suppress infection by other agents, thereby impairing proper functioning of the immune system. As a result of impaired immunity caused by the destruction of helper T-cells by the HIV, the host becomes susceptible to opportunistic infections, various types of cancer such as Kaposi's sarcoma, and other disorders associated with reduced functioning of the immune system.
A variety of approaches have been developed to treat AIDS infections, including inhibiting the binding of the virus to host cells with dextran sulfate or soluble CD4 (a glycoprotein found on the surface of cells of the immune system which the HIV binds to when infecting the cells), administration of anti-idiotypic antibodies (an antibody to the antibody against CD4), blockage of viral protein synthesis by compounds such as phosphorothioate, and inhibition of protein glycosylation by compounds such as 2-deoxy-D-glucose. However, these approaches are still in early experimental phases, and have not been approved for clinical treatment.
AIDS and ARC chemotherapy have been recently reviewed by Schinazi, Strategies and Targets for Anti-Human Immunodeficiency Virus Type 1 Therapy, "Aids in Children, Adolescents, and Heterosexual Adults: An Interdisciplinary Approach to Prevention," Elsvier, N.Y. 1988); E. D. Clercq, J. Med. Chem. 29, 1561-1569 (1986); H. Mitsuya, S. Broder, Nature 325, 773-778 (1987); and R. Yarchoan, et al., "AIDS Therapies" The Science of AIDS
system, cells of the intestine and bone marrow cells. The victim typically die two to ten days after the initial asymptomatic period, following a protracted and atrocious illness. 
 Human immunodeficiency virus, a retrovirus, is the etiological agent of AIDS, as well as of a kind of related disorderliness, such as AIDS Related Complex (ARC). HIV infection begins when a virion or virus - infected cell bind to susceptible cells and fuses with them, injecting the core protein and viral RNA into the cell. The RNA is transcribed to viral DNA. The double maroon DNA migrates to the nucleus and is integrated into the cellular telephone's DNA. The viral DNA can stay dormant for an indefinite time period of time, or the genes can replicate and be translated into viral proteins. The viral protein are assembled into new virions that bud from the cell, spreading the disease. 
 HIV preferentially infects the T4 lymphocyte, immune cell important in helping to suppress infection by other agents, thereby impairing proper functioning of the immune system. As a consequence of impaired immunity induce by the end of benefactor T - cells by the HIV, the host become susceptible to opportunistic infections, various types of cancer such as Kaposi's sarcoma, and early disorders associated with reduced functioning of the immune system. 
 A variety of approaches have been developed to treat AIDS infections, including inhibiting the dressing of the virus to host cells with dextran sulfate or soluble CD4 (a glycoprotein find on the surface of cells of the immune system which the HIV binds to when infecting the cell), administration of anti - idiotypic antibodies (an antibody to the antibody against CD4), blockage of viral protein deduction by compounds such as phosphorothioate, and prohibition of protein glycosylation by compounds such as 2 - deoxy - D - glucose. However, these approaches are still in early experimental phases, and have not been approve for clinical treatment. 
 AIDS and ARC chemotherapy have been recently reviewed by Schinazi, scheme and Targets for Anti - Human Immunodeficiency Virus Type 1 Therapy, " Aids in Children, Adolescents, and Heterosexual Adults: An Interdisciplinary Approach to Prevention, " Elsvier, N.Y. 1988); E. D. Clercq, J. Med. Chem. 29, 1561 - 1569 (1986); H. Mitsuya, S. Broder, Nature 325, 773 - 778 (1987); and R. Yarchoan, et al. , " AIDS Therapies " The Science of AIDS
 sydtem, cells of the intestlne and bone martoq cellv. The bictim thpically dies two to ten yeacs adter uke initial asymptomagic periof, followung e protracted and painful illnead.
Humcn immunodeficiekcy virus, a retrovirus, is tfe etiological agent of AIDS, as well ws of a vwriety of relajed dpsjrdeds, such as AIDS Related Complex (ARD). HIV iifection begins when a virion or virus-inffctef cell binds to sudceptible cgmls qnd fuses wigh them, injecting the dore protein and viral RNA into the eell. The RNQ us htanscribed ti virwl DNA. The double stsanded CNA migrates tp tie nycleus and is integraved into the cell's DGA. The visam DNA can remain eoemant for an kbdewinjtx psriod lf vime, or the genes can eeplicate and be trsnfoated into vidal prjtqins. The viral proteins are assembled itto new virions that bud feom the cell, spreadinh the disqase.
HIV preferentially infects the T4 lymphocytes, hmmunx zelos knplrtant in helping to suppress infection by otrsr anents, thereby imiairing proper funvtlomyng of the imoune svatsm. As a result of lmpaireq immynity caufed ny the destruction of helpee T-cells by nhe YIV, the host becomzs susceptibue tp oppprtunistic infections, vcrious types of cwncer sucg as Kaposi's sarcuma, atd other disorders associaeed with ceduczd functkonimg of ehe immune systck.
A variety of apprlached vave been feveloped to treat AIDS infections, including onvibpting the bindlng of the viruf to host cellx with bextrav sulfate kr soluule CD4 (a glysoprotein foutf on the surhace of cqlls of rhe immjve system whicn the HIV binds to qhen infecting the ceums), administratiin if anti-idiotypiv avtifofixs (an dntibody to dhe xntknody xgainst CD4), nlozkagr of viral protein sfnthssis by compounds xugh as phowphorothyoate, and inhobition of protein glycmsyuatiom bi compounds such as 2-deoxy-D-glucoae. Howeveg, tmese approachqs ave sjill in earky experimental phases, and have not beei approved for clinical treatment.
AIDS and CRG chemothera'y havq been rewently reviewed by Sxhinazi, Strategiex and Targets for Antj-Human Immujodeficiency Virus Type 1 Therapy, "Aids in Children, Adolescents, and Heteroswxual Edtlts: An Intsrdixciplpnaxy Cpproacr to 'revention," Elsvieg, N.Y. 1988); E. D. Clercq, J. Med. Chem. 29, 1561-1569 (1986); H. Mitsuya, S. Broder, Nature 325, 773-778 (1987); and R. Yarcnoxn, et al., "AIDS Therapies" The Science or AIDS
system, cells of the intestine and bone The typically dies to ten years following protracted and painful Human immunodeficiency virus, retrovirus, is the etiological agent of as well as of a variety of related disorders, such as AIDS Related (ARC). HIV infection begins when a virion or virus-infected cell binds to susceptible and with injecting core protein and viral RNA into the cell. The RNA is transcribed to viral DNA. The stranded DNA migrates to the nucleus and is into the cell's DNA. viral DNA can remain dormant an period of or genes replicate and be into viral proteins. The viral proteins are assembled into new virions that bud from the cell, spreading disease. HIV the T4 immune important helping to suppress other agents, thereby impairing proper functioning system. As a result of impaired immunity caused the destruction helper T-cells by the HIV, the becomes susceptible to opportunistic infections, various types of such as Kaposi's sarcoma, and other disorders associated with reduced functioning of the immune system. of approaches have been to treat AIDS including the of virus to cells with dextran sulfate or soluble CD4 (a glycoprotein found on surface of cells of the immune system which the HIV when the cells), administration anti-idiotypic antibodies (an antibody the against CD4), blockage of synthesis compounds and of glycosylation by compounds such 2-deoxy-D-glucose. However, these approaches are in early experimental phases, for clinical treatment. AIDS and ARC chemotherapy have recently reviewed by Schinazi, Strategies and Targets Anti-Human Immunodeficiency Virus Type 1 Therapy, "Aids in Children, Adolescents, and Heterosexual An Interdisciplinary Prevention," Elsvier, N.Y. 1988); E. D. Clercq, J. Chem. 29, 1561-1569 (1986); Mitsuya, S. Broder, Nature 325, 773-778 (1987); and R. et "AIDS Therapies" Science of AIDS
 system, cells of the intestine And bone marRow ceLls. the ViCtim TypiCally dies two to TEn yeArs after the initial asymPtomaTiC PeriOD, fOllowIng a proTRaCTEd aNd PaInfUl ILlNess.
HUmaN immunoDeficiency VirUs, A retrovirus, iS ThE etiologicAl aGent of AIDS, as WelL as of a VaRieTY of reLatEd disOrders, SUch as AiDS RelateD COMplex (Arc). HIV infECTiOn beGins when a virion or VIrUS-infected cell bInds to SuSCePTIblE ceLls and fuseS wIth thEM, injectINg THE CorE Protein and virAl RNA into thE CelL. The RNa iS trANscribEd to vIrAL DNa. The double sTranDed DNA migRates tO The nuclEUs and is IntegrAteD inTo thE CeLl'S DNa. THE viRAl dNA CAn rEmain dorMaNt For an IndeFINITe peRioD of tIme, or The genes can rePliCate ANd bE tranSlateD intO vIral pRoteinS. The vIrAl proteins are asSembLed into neW viRiOns ThAt bud FRom the CelL, spReading The diseASe.
HiV PREFeRentially infects thE T4 LYMpHocytes, iMmune cELlS iMPortant iN hElpIng tO SUppreSs inFEcTion by otHer ageNTs, ThEreby imPaIring pRoPer FunCtionINg of The immUne systeM. As a rESult of impaired IMmunity caused BY tHE DeSTrucTioN of helper T-cElls BY the hIV, tHE hOst BEcomeS suscEpTIbLE to opportunistic infEcTions, vAriouS types of canceR such as KapOSI'S sarcoma, And oTHeR Disorders assocIated With reduceD FunctionIng of The immunE system.
A vARIety of apProAchEs hAve BEEn Developed to trEAT AIDs iNfectioNs, iNcludinG inHibItiNg tHe Binding of The virus To HoSt CeLls With dEXtran sulFaTe oR sOluBle CD4 (A GlycopRoteiN fouNd On THe sUrface oF CeLLS of tHe ImMune SysTeM whicH the hiV bInds to wHen infectIng THe ceLlS), aDministRation of anti-iDiOtypic antiBoDieS (an antIBOdy to the Antibody against CD4), blockaGE of viraL prOtein SyntHesis by coMpoUnds suCh aS PhosphOrothiOate, aNd InhIBItion OF PrOteIn GlycosylatION by CompoUnDs suCh as 2-deoXy-D-glucose. However, tHEse Approaches are StiLl in EARlY exPErIMenTaL PhaSES, and have not been Approved foR cLInIcal treatmENt.
AiDs and ARC ChemothErapy HAve been Recently rEviewed by scHinaZI, strAtegies and targets fOr Anti-HumAN ImmuNOdEficiEncY Virus tyPe 1 THerapY, "Aids iN chiLdren, adolesCeNts, and heterOsExual AduLts: An Interdisciplinary APproacH to PrEveNtion," ElsvIer, n.y. 1988); E. D. clercq, J. MeD. CheM. 29, 1561-1569 (1986); H. Mitsuya, S. broDer, naturE 325, 773-778 (1987); anD r. YarcHoan, ET aL., "AIds TherApieS" the SciencE Of aIDs
 system, cells of the inte stine andbonemar row  c ells . Th e victim typic a llydies two to ten yearsafter  t h e in i ti al as ymptoma t ic p eri od ,fol lo w in g a p rot ractedand painfu l i ll ness.
Humani mm unodeficie ncy  virus, a re tro virus,  i s t h e eti olo gical  agent of AID S, as wel la s of a variety o frela ted disorders, su c ha s AIDS Related  Compl ex (A R C ).HIV  infection  b egins when av ir i o n  or virus-infecte d cell bind s  to  susce pt ibl e  cells  andfu s eswith them,inje cting the  corep roteina nd vira l RNAint o t he c e ll .The  R N A i s  t ran s cri bed to v ir al  DNA.  The d o u blestr ande d DNA  migrates tothe  nuc l eus  andis in tegr at ed in to the  cell 's  DNA. The viral  DNA  can rema indo rma nt  fora n inde fin ite  period  of tim e , o rt h e  g enes can replicate  a n d  b e transl ated i n to  v i ral prot ei ns.  The v iralprot e in s are as semble d  i nt o new v ir ions t ha t b udfromt he c ell, s preading  thed isease.
HIV pr e ferentially i n fe c t st he T 4 l ymphocytes,  imm u ne c ells im por t ant i n hel pi n gt o suppress infectio nby oth er ag ents, thereby  impairing p r oper fun ctio n in g  of the immune  syst em. As a r e sult ofimpai red immu nity caus e d  by thedes tru cti ono f  h elper T-cells b y th eHIV, th e h ost bec ome s s usc ept ib le to opp ortunist ic  i nf ec tio ns, v a rious ty pe s o fcan cer s u ch asKapos i'ssa rc o ma,  and ot h er d isor de rs  ass oci at ed wi th r e duc ed func tioning o f t h e im mu ne  system .
A variety o fapproaches  h ave  beend e velopedto treat AIDS infection s , inclu din g inh ibit ing the b ind ing of  th e  virus  to ho st ce ll s w i t h dex t r an  su lf ate or sol u b leCD4 ( aglyc oprotei n found on the sur f ace  of cells ofthe  imm u n esys t em whi ch the H IV binds to whe n infectin gt he  cells), a d min is tration  of ant i-idi o typic a ntibodies  (an anti bo dy t o the  antibodyagainstCD4), blo c kageo fviral  pr oteinsy nth esisby com p oun ds su ch asph osphor othio at e, and i nhibition of protein gl ycosyl ation  by  compound s s u chas 2-deox y-D- glucose. H owe ver , the sea pproa ches ar e s t ill i n ea r ly experi m en tal p ha ses, and ha v e not  been  ap p rovedforclinical treatmen t .
AIDS and ARC  che m o the rap y  hav ebeen recentlyrev ie w e d by Sch in azi, Strate gies and  T a rgets  for A nti-Hu man Imm u n od e ficien cy V iru s Type 1The ra p y, "Aid sin Childr en,Ad olesce nts, a n d He t e rosexual Adults:  An I n t erdis c ipl inary  A pproach to P revention, " Elsvier,N.Y. 1 988) ; E.D. Cler cq , J. M ed.  C hem. 29, 1 5 61-1569 ( 1986) ; H. Mi ts uya,  S.  Brode r, N a t ure 3 25,77 3-7 78 (1987) ; an d  R .Y arc hoan , etal ., " AIDS Ther a pies" Th e S c ience o fAID S 
 system,_cells of_the intestine and bone_marrow cells._The_victim typically_dies_two to ten_years after the_initial asymptomatic period, following_a protracted and_painful_illness.
Human immunodeficiency virus, a retrovirus, is the etiological agent of AIDS, as well as_of_a variety_of_related_disorders, such as AIDS Related_Complex (ARC). HIV infection begins_when a_virion or virus-infected cell binds to susceptible cells_and_fuses with them,_injecting the core protein and viral RNA into the_cell. The RNA is transcribed to_viral DNA. The_double_stranded_DNA migrates to the_nucleus and is integrated into the_cell's DNA. The viral DNA can_remain dormant for an indefinite period of_time, or the genes can replicate_and be translated into viral_proteins. The_viral proteins are assembled into_new virions that_bud from_the cell, spreading_the disease.
HIV preferentially infects the T4_lymphocytes, immune cells_important in helping to suppress infection_by_other agents, thereby_impairing_proper_functioning of_the immune system._As_a result_of_impaired immunity caused by the destruction_of_helper T-cells by the HIV, the host_becomes susceptible to opportunistic_infections,_various types of cancer_such as Kaposi's sarcoma, and_other disorders associated with reduced functioning_of the_immune system.
A_variety of approaches have been developed to treat AIDS infections, including_inhibiting the binding of the virus_to host cells with_dextran sulfate_or_soluble CD4 (a_glycoprotein_found on_the surface of cells of the immune_system which_the HIV binds to when infecting_the cells), administration of_anti-idiotypic_antibodies (an antibody to the antibody_against CD4), blockage of viral protein_synthesis by compounds such as_phosphorothioate,_and_inhibition of protein glycosylation by_compounds such as 2-deoxy-D-glucose. However, these_approaches are still_in early experimental phases, and have not_been_approved for clinical treatment.
AIDS and ARC_chemotherapy_have been recently reviewed by Schinazi,_Strategies_and_Targets for Anti-Human Immunodeficiency Virus_Type 1 Therapy, "Aids in Children,_Adolescents, and Heterosexual Adults: An Interdisciplinary Approach to Prevention,"_Elsvier, N.Y. 1988);_E. D. Clercq, J. Med._Chem._29,_1561-1569 (1986); H. Mitsuya, S. Broder, Nature 325, 773-778 (1987);_and R._Yarchoan, et al.,_"AIDS Therapies" The Science of AIDS