New Approaches in The Treatment of AIDS

Available Online at www.ijptb.com Singh A.,et al. Int. J. Pharm. Technol. Biotechnol.
2021; 8(3):83-101
ISSN:2394-2371
REVIEW PAPER
CODEN (USA):IJPTIL
New approaches in treatment of AIDS

Amandeep Singh1*, Nisha A Bhatt2, Amar jit Singh3, Akshit Sinha3, Abhay Goswami3
1
Professor, Dev Bhoomi Institute of Pharmacy & Research, Dehradun, Uttrakhand, India
2
Associate Professor, Dev Bhoomi Institute of Pharmacy & Research, Dehradun, Uttrakhand, India
3
Research Scholar, Dev Bhoomi Institute of Pharmacy & Research, Dehradun, Uttrakhand, India
*Corresponding Author: Prof. (Dr) Amandeep Singh
ABSTRACT
At present there is no cure available for HIV/AIDS.Though there are drugs which help people prolong
their life expectancy and live a normal life. This review article gives the brief insight about the history
of this disease, its first reported case, the transmission of this disease and how it dosen’t spread,
etiology of disease, its pathophysiology along with clinical manifestations, detection of this disease
and the antiretroviral therapy. The accessible antiretroviral (ARV) drugs for the treatment of HIV have
extended since old days. Novel methods of ARVs with new instruments of activity have been
endorsed, including ibalizumab-uiyk and fostemsavir. There have additionally been endorsements of
blend tablets of already accessible medications, for example, bictegravir/emtricitabine/tenofovir
alafenamide and dolutegravir/lamivudine. At last, there has been a development in endorsed signs for
already accessible ARVs themselves, for example, emtricitabine/tenofovir alafenamide for use in pre-
exposure prophylaxis. Scientists are in a race to find a cure for this deadly disease .Research are going
on globally to counter this disease. This review article also give a brief about safety measures for
controlling this disease.
Keywords: - Antiretroviral Therapy, HIV, AIDS, Transmission, Detection, Treatment.
INTRODUCTION
AIDS-Acquired Immunodeficiency Syndrome:This lethal sickness is brought about by HIV (Human
Immune Deficiency Virus) contamination and is portrayed by the decrease in CD4+ T-cells. This
generally means the individual who is tainted by this infection fosters a powerless insusceptible
framework which opens an entryway for the weakness to other illness which might be dangerous. HIV
causes AIDS and meddles with the body's capacity to battle contaminations. [6,13]
FIRST CASES OF AIDS
*Corresponding Author:
Prof. (Dr) Amandeep Singh In 1981 US detailed the primary instance of AIDS. The
Professor, Dev Bhoomi Institute of Pharmacy &
Research, Dehradun, Uttrakhand, India centre for disease control announced gay men in Los
E.Mail: jd.pharmacy@dbgidoon.ac.in Angeles had new, puzzling/mysterious ailment which
Article Published: July-Sept. 2021
looked like pneumonia. It was in 1982, when wellbeing
Cite this article as:
Singh A, Bhatt NA, Singh A, Sinha A, Goswami local area named this strange sickness as AIDS.
A. New approaches in treatment of AIDS. Int. J.
Pharm. Technol. Biotechnol. 2021; 8(3): 83-101. HISTORY
International Journal of Pharmaceutical Technology and Biotechnology 83

Available Online at www.ijptb.com Singh A.,et al. Int. J. Pharm. Technol. Biotechnol. 2021; 8(3):83-101
Researchers believe that HIV initially came from a virus from chimpanzees in africa and from that
point it was communicated to people through the exchange of blood through chasing. Over many years
the infection continued spreading across the globe following travel and blood industry. [2]
HIV DOSEN’T SPREAD BY
1) Shaking hands with someone who has HIV/AIDS
2) Hugging someine who has HIV/AIDS
3) Sharing a living space
4) Kissing and touching
5) Sharing foods and utensils
6) Mosquitos and other insects
7) Toilet seats
Fig.1: Non-Transmission of HIV

HIV TRANSMISSION
HIV is communicated through the body liquids like blood, semen, rectal fluids, vaginal liquids, and
bosom milk. The transmission happens while contaminated individual mucous layer in the rectum,
vagina, penis interacts with another person. HIV can be spread during unprotected butt-centric or
vaginal sex. Oral sex additionally posess a danger of getting of the HIV if there are mouth ulcers,
bleeding gums, genital wounds and transmission can happen during discharge. IV drug use - sharing a
needle/syringe with the infected person also causes the transmission.Blood transfusion- Today’s blood
transfusion are mostly safe as they are tested. But before 1985 it was a major cause of
transmission.Mother to infant- There are medications which help reduce the risk of contracting disease
still HIV/AIDS can be passed on so it is recommended to get test done for all pregnant women.Sharing
a razor blade also causes the transmission if one is infected.[12]

Fig.2: Transmission of HIV

ETIOLOGY
HIV is the causative specialist for AIDS. HIV unwellness is brought about by contamination with
HIV-1 or HIV-2, which are retroviruses inside the Retroviridae family, Lentivirus genus . The chief
normal kind is HIV-1 and is at fault for the overall pestilence . [3,5]
Albeit unmistakable HIV-1 and HIV-2 share a few antigens. Actually like most creature infection, the
HIV-1 molecule is round partner degreed contains an electrone-thick, cone shaped center encased by a
supermolecule include got from the host cytomembrane. The infection center contains:
 the significant capsid supermolecule,
 nucleoscapsid supermolecule and 2 duplicates of genomic RNA and
 the three infective specialist compounds protease, polymerase and integrase
Fig.3: Electron microscopy of HIV-1 virions

Fig.4: Genomic layout of HIV-1 and HIV-2

PATHOPHYSIOLOGY
1. Attachment
2. Transcription of RNA-directed DNA polymerase
3. Blending
4. Translation
5. Viral protease
6. Assembly and budding.
SYMPTOMS
1. Swollen lymph hubs, Fever, Night Sweats, Rash, Mouth Ulcers, Muscle Aches, Fatigue, Chills,
Dry Cough, Loss of hunger, Nausea,Watery Diarrhea, Pneumonia,Weight misfortune,
Difficulty gulping.
2. A relentless decline in CD4 T-cells is the most quantifiable part of safe framework estruction.
[17]
3. Vulnerability to other various illness
4. Infection because of protozoa
5. Infection because of helminths
6. Infections because of microorganisms
7. Infections because of infection
8. Neurological illness
DETECTION
 Antigen/antibody tests
 Antibody tests
 Nucleic acid analyses
 CD4 T cell count
 Viral load (HIV RNA)
 Drug resistance
 ELISA

Antigen/antibody tests:
This test includes the drawing of blood from veins. HIV (antigen) can't be distinguished in beginning
of openness yet following not many weeks it very well may be identified, Antibodies delivered
accordingly of body against this infection takes weeeks to month be recognizable, this test can require
2 a month and a half after openness to get positive.[19,21]
Antibody tests:
Following of immune response against HIV in blood or spit is performed here, it can require 3-12
weeks after openness to infection.
Nucleic basic analyses:
This test search for presence of HIV infection in the blood. In the event that you were presented to
HIV inside couple of weeks specialist will suggest this test NAT.
CD4 T cell count:
These are those cells white platelets which is assaulted by the HIV and gets annihilated by HIV. HIV
disease keep on advancing despite the fact that you have no sign and manifestations and cause AIDS
when CD4 T cell tally goes under 200. [23]
Viral load:
This test is done to get the estimation of sum if infection present in the blood plasma. A higher the
viral burden foreseeing quicker movement of sickness. [6]
This test expects to diminish the viral burden to imperceptible after inception of HIV treatment and
consequently lessening the odds of other artful sickness/disease of any kind.
Drug resistance:
There are cases that a few strains of HIV is impervious to prescriptions . This test assists specialist
with deciding explicit safe infection and treat in like manner.
ELISA:
Catalyst Linked Immuno Sorbent Assay, in this tests a patient’s blood test for antibodies.
HIV TREATMENT
With the consistent improvement in present day science there's still no solution for HIV except for
researchers are making a decent attempt to discover a fix , yet there is advancement in therapy when
contrasted with decade before because of headway in clinical science individuals would now be able
to carry on with a more extended everyday routine with dynamic experiences with HIV . This
treatment point in diminishing the viral burden to least so a test can't recognize any HIV signs,
because of this individual can remain solid and draw out existence without taking a chance with
other's life. Accepting medication as specialist endorsed will likewise help infection from changing

and getting impervious to the medications. On the off chance that safe is created, there can be limit in
treatment alternative and shots at spreading the infection is almost certain . [24,28]
ART (Antiretroviral Therapy)
These are those medication which help in treatment of HIV and called antiretroviral drugs. Keeping
the measure of HIV in blood as low as workable for as far as might be feasible. Expanding or settling
the quantity of CD4 cells. Bringing down the danger of HIV creating opposition.(13.31)
Three essential techniques for approach in the treatment:
 Hindrance of viral replication.
 Immunization to invigorate a more powerful invulnerable reaction.
 Rebuilding of the insusceptible framework with immuno modulators.
CLASSIFICATION OF ART DRUGS
 Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
 Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
 Protease Inhibitors (PIs)
 Integrase Inhibitors
 Fusion Inhibitors
 gp120 Attachment Inhibitor
 CCR5 Antagonist
 Post-Attachment Inhibitor or Monoclonal Antibody
 Pharmacologic Enhancers, or "Drug Boosters"
 Fixed-Dose Combinations
 PrEP Medication
Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
Mechanism of Action
Nucleoside analogs are additionally alluded to as nucleoside invert transcriptase inhibitors. Their
objective is the HIV protein turn around transcriptase. Going about as elective substrates or "bogus
structure blocks", they contend with physiological nucleosides, varying from them exclusively by a
minor alteration in the sugar particle. The joining of nucleoside analogs cuts short DNA blend, as
phosphodiester extensions can at this point don't be worked to balance out the twofold strand. [19]
Nucleoside analogs are changed over to the dynamic metabolite solely after endocytosis, whereby they
are phosphorylated to triphosphate subordinates. AZT and d4T are thymidine analogs, while ddC, FTC
and 3TC are cytidine analogs. Mixes containing AZT in addition to d4T, ddC in addition to 3TC or
FTC in addition to 3TC are hence silly, since the two medications would go after similar bases. ddI is

an inosine simple, which is changed over to dideoxyadenosine; abacavir is a guanosine simple. There
is a serious level of cross obstruction between nucleoside analogs.
Nucleoside analogs are not difficult to take, and once-every day dosing is adequate for the greater part
of these medications. By and large bearableness is genuinely acceptable. Regular protests during the
principal weeks are weariness, cerebral pain and gastrointestinal issues, which range from gentle
stomach uneasiness to sickness, retching and the runs. The gastrointestinal protests are effortlessly
treated apparently.[6,17]
In any case, nucleoside analogs can cause a wide assortment of long haul results, including
myelotoxicity, lactate acidosis, polyneuropathy and pancreatitis. In spite of the fact that lipodystrophy
was at first connected only to treatment with protease inhibitors, may problems of lipid digestion
(particularly lipoatrophy) are currently additionally credited to nucleoside analogs. Long haul results
that are presumably identified with mitochondrial poisonousness were first portrayed in 1999 .
Mitochondrial work requires nucleosides. The digestion of these significant organelles is upset by the
consolidation of bogus nucleosides, prompting mitochondrial degeneration. Later clinical and logical
information demonstrates that there are most likely significant contrasts between singular medications
as to mitochondrial harmfulness: d4T, for instance, is more poisonous than abacavir. [23]
Nucleoside analogs are wiped out for the most part by renal discharge and don't cooperate with drugs
that are used by hepatic proteins. There is accordingly, minimal potential for connection. Nonetheless,
substances like ribavirin, which is likewise enacted by intracellular phosphorylation, may cooperate
with nucleoside analogs of AZT, d4T and ddI.
 Abacavir, or ABC (Ziagen)
 Didanosine, or ddl (Videx)
 Emtricitabine, or FTC (Emtriva)
 Lamivudine, or 3TC (Epivir)
 Stavudine, or d4T (Zerit)
 Tenofovir alafenamide, or TAF (Vemlidy)
 Tenofovir disoproxil fumarate, or TDF (Viread)
 Zidovudine or ZDV (Retrovir)
Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Mechanism of action and efficacy
Similarly as with the nucleoside analogs, the objective catalyst of NNRTIs is converse transcriptase.
NNRTIs were first depicted in 1990. As opposed to the NRTIs, they are not "bogus" building blocks,
but instead tie straightforwardly and non-seriously to the protein, at a situation in closeness to the

substrate restricting site for nucleosides. The subsequent complex squares the impetus actuated
restricting site of the opposite transcriptase, which would thus be able to tie less nucleosides, easing
back polymerization down altogether. Rather than NRTIs, NNRTIs don't need enactment inside the
cell. [28]
The three at present accessible NNRTIs - nevirapine, delavirdine and efavirenz - were presented
somewhere in the range of 1996 and 1998.
This was because of the early perception that useful monotherapy with NNRTIs, for example the
simple expansion of a NNRTI to a weak routine, showed for all intents and purposes no impact. There
were likewise beginning troubles in managing the dangerous obstruction profile of NNRTIs. The
danger of cross-opposition is high, and it can grow quickly; one point change at position 103 (K103N)
of the hydrophobic restricting site is sufficient to wipe out the whole medication class! Opposition has
now even been depicted in moms taking a solitary portion of nevirapine upon entering the world for
maternal transmission prophylaxis. This marvel isn't uncommon. In two enormous examinations, the
recurrence of NNRTI transformations following perinatal nevirapine prophylaxis was somewhere in
the range of 14 and 32
 Cabotegravir/rilpivirine (Cabenuva)
 Delavirdine or DLV (Rescripor)
 Doravirine, or DOR (Pifeltro)
 Efavirenz or EFV (Sustiva)
 Etravirine or ETR (Intelence)
 Nevirapine or NVP (Viramune)
 Rilpivirine or RPV (Edurant)
Protease Inhibitors (PIs)
Mechanism of action and efficacy
The HIV protease cuts the viral gag-pol polyprotein into its utilitarian subunits. Hindrance of the
protease, forestalling proteolytic joining and development, prompts the arrival of infection particles
that can't taint new cells. With information on the atomic construction of the protease encoded by the
infection, the principal protease inhibitors were planned in the mid nineties; these substances were
changed so that they fit precisely into the compound dynamic site of the HIV protease.
Yet, even on account of PIs, the distinctions are not so critical as to totally bargain singular individuals
from this class. Two special cases must be referenced: the hard gel case saquinavir-HGC and ritonavir
all alone. Supported PI regimens are apparently more compelling. [12,34]

Aside from gastrointestinal results and high pill trouble, all PIs utilized in long haul treatment can be
involved in lipodystrophy and dyslipidemia. More modest randomized investigations have shown that
height of lipid levels is more articulated in ritonavir-containing regimens (full, not supporter portion)
than with saquinavir or nelfinavir . Moreover, there might be huge medication associations on
ritonavir and with supported regimens. Sexual brokenness has additionally been ascribed to PIs,
despite the fact that information is uncertain. There is a serious level of cross-opposition between
protease inhibitors, which was portrayed even before PIs were put available. All PIs are inhibitors of
the CYP3A4 framework and connect with various different medications. Ritonavir is by a wide
margin the most grounded inhibitor, saquinavir likely the most fragile.
These medications block a protein that tainted cells need to assemble new HIV infection particles.
 Atazanavir or ATV (Reyataz)
 Darunavir or DRV (Prezista)
 Fosamprenavir or FPV (Lexiva)
 Indinavir or IDV (Crixivan)
 Lopinavir + ritonavir, or LPV/r (Kaletra)
 Nelfinavir or NFV (Viracept)
 Ritonavir or RTV (Norvir)
 Saquinavir or SQV (Invirase, Fortovase)
 Tipranavir or TPV (Aptivus)
Integrase Inhibitors
These prevent HIV from making duplicates of itself by impeding a key protein that permits the
infection to place its DNA into the sound cell's DNA. They're additionally called integrase strand
move inhibitors (INSTIs).
Integrase inhibitors depend on the way that HIV needs integrase to duplicate. These medications
prevent HIV from having the option to make integrase. Without the assistance of this protein, HIV
can't assume control over the T cells to duplicate itself.[21]
With a blend of other HIV drugs, integrase inhibitors can help monitor HIV.
The U.S. Food and Drug Administration (FDA) endorsed the utilization of integrase inhibitors in
2007. The integrase inhibitors presently available include:
 raltegravir (Isentress)
 dolutegravir (Tivicay)
 elvitegravir (accessible in mix with different medications; not, at this point accessible alone)
 bictegravir (accessible in mix with different medications; not accessible alone)

 Dolutegravir and elvitegravir are accessible in the accompanying blend drugs:

 Genvoya (elvitegravir, emtricitabine, tenofovir alafenamide fumarate, cobicistat)
 Stribild (elvitegravir, emtricitabine, tenofovir disoproxil fumarate, cobicistat)
 Triumeq (dolutagravir, abacavir, lamivudine)
 Juluca (dolutegravir, rilpivirine)
 Biktarvy (bictegravir, emtricitabine, tenofovir alafenamide fumarate)
Integrase inhibitors are frequently utilized as the underlying drugs for treating HIV. Normally, they're
utilized with different medications, regularly in one mix pill.
Different medications in these mix pills help meddle with alternate ways that HIV works. The joined
activity of these medications in this single tablet system helps stop HIV through various ways on the
double
Fusion Inhibitors
Inhibitors of the combination of HIV to have cells, forestalling viral passage. This incorporates
intensifies that block connection of HIV ENVELOPE PROTEIN GP120 to CD4 RECEPTORS. In
contrast to NRTIs, NNRTIs, PIs, and INSTIs, which work on contaminated cells, these medications
block HIV from getting inside sound cells.
 Enfuvirtide, or ENF or T-20 (Fuzeon)
Enfuvirtide is the lone authorized combination inhibitor to date. This moderately new class of against
retroviral drug works by obstructing viral section into have cells. Enfuvirtide is a 36 amino corrosive
manufactured peptide dependent on the extracellular locale of the transmembrane protein gp41. This
medication hinders the conformational change of the HIV envelope spike needed to uncover the
fusogenic space of gp41. The infection can't meld with the host cell layer and subsequently can't enter
the cell. Weaknesses of enfuvirtide are that it is presently over the top expensive and hard to fabricate,
and should be conveyed by subcutaneous infusion.[12.18] Enfuvirtide is suggested for HAART in
patients whose viral separates show protection from different classes of inhibitors. Other combination
inhibitors are going through clinical testing.
Gp120 Attachment Inhibitor
This is another class of medication with only one prescription, fostemsavir (Rukobia). imperviousIt is
for grown-ups who have attempted various HIV meds and whose HIV has been to different
treatments. It focuses on the glycoprotein 120 on the outside of the infection, preventing it from
having the option to connect itself to the CD4 T-cells of your body's invulnerable framework.

Connection inhibitors are a class of medications that tight spot to the gp120 protein on the external
surface of HIV, keeping HIV from restricting to and entering CD4 T lymphocytes (CD4 cells).
Connection inhibitors are important for a bigger class of HIV drugs called section inhibitors. [7]
 Fostemsavir
The new highlighted preliminaries of a few HIV drugs with methods of activity unique in relation to
the standard classes. Notwithstanding the general achievement of antiretrovirals (ARVs), there stay a
minority of individuals who, because of the advancement of obstinate HIV drug obstruction, actually
need what used to be designated "rescue drugs".
Two are section inhibitors. Just as ibalizumab (Trogarzo), effectively announced here, the gathering
caught wind of fostemsavir. This medication, initially called BMS-663068, prevents HIV from
entering cells not by appending to the CD4 receptor on cells, as ibalizumab does, or to the CCR5 co-
receptor, as maraviroc does. Rather it joins itself to the infection, explicitly to the gp120 particle, the
'spikes' on the outside of HIV that are the methods for viral section into the cell. [11]
With the goal for HIV to bolt onto the CD4 receptor and breaker with the cell film, the gp120 protein
unfurls into a three-section even construction (a trimer). This change is important for it to join itself to
the host CD4 receptor. Temsavir – which is the thing that fostemsavir becomes in the body – lodges
itself into the inner construction of gp120 right now of its parting separated and forestalls the
interaction of viral connection
CCR5 Antagonist
CCR5 inhibitors are another class of antiretroviral drug utilized in the treatment of human
immunodeficiency infection (HIV). They are intended to forestall HIV contamination of CD4 T-cells
by obstructing the CCR5 receptor. At the point when the CCR5 receptor is inaccessible, 'R5-jungle'
HIV (the variation of the infection that is normal in prior HIV disease) can't draw in with a CD4 T-cell
to taint the cell. Maraviroc, the main medication from this class to be advertised.
 Maraviroc
Maraviroc, or MVC , likewise stops HIV before it's anything but a sound cell, yet in an unexpected
path in comparison to combination inhibitors. It's anything but a particular sort of "snare" outwardly of
specific cells so the infection can't connect.
Post-Attachment Inhibitor or Monoclonal Antibody
Post-connection inhibitors are a class of medications that tight spot to the CD4 receptor on a host CD4
cell. This squares HIV from joining to the CCR5 and CXCR4 coreceptors and entering the phone.
Post-connection inhibitors are important for a bigger gathering of HIV drugs called passage inhibitors.
This is another class of antiviral drug explicitly for grown-ups living with HIV who have attempted

numerous HIV meds and whose HIV has been impervious to different treatments. Ibalizumab blocks
your body's HIV tainted cells from spreading the infection into those which are uninfected. It is given
by IV [7,19].
 Ibalizumab
Ibalizumab is an adapted monoclonal neutralizer (mAb) that ties to extracellular area 2 of the CD4
receptor. The ibalizumab restricting epitope is situated at the interface between areas 1 and 2, inverse
from the limiting site for significant histocompatibility complex class II atoms and gp120 connection.
Ibalizumab doesn't restrain HIV gp120 connection to CD4; nonetheless, its postbinding
conformational impacts block the gp120-CD4 complex from collaborating with CCR5 or CXCR4 and
subsequently forestalls viral passage and combination.
Pharmacologic Enhancers, or "Drug Boosters"
Supporter drugs are utilized to 'help' the impacts of protease inhibitors and some other antiretrovirals.
Adding a little portion of a supporter medication to an antiretroviral makes the liver separate the
essential medication all the more leisurely, which implies that it stays in the body for longer occasions
or at more significant levels.
Ritonavir (RTV), taken in a low portion, builds blood levels of lopinavir (LPV) and the medication
LPV/r (Kaletra).
Cobicistat (Tybost) does likewise in blend with atazanavir, darunavir, elvitegravir.
Atazanavir + cobicistat, or ATV/c (Evotaz)
 Darunavir + cobicistat, or DRV/c (Prezcobix)
 Elvitegravir + TDF + FTC + cobicistat, or EVG/c/TDF/FTC (Stribild)
 Elvitegravir + TAF + FTC + cobicistat, or EVG/c/TAF/FTC (Genvoya)
Since these "drug promoters" can build the degrees of different medications and cause possible
damage, you ought to consistently enlighten your PCP concerning the prescriptions you are taking.
Fixed-Dose Combinations
Some medication producers set up explicit prescriptions into a solitary pill so they're simpler to take,
including:
Integrase strand move inhibitor (INSTI)- based:
 Bictegravir + tenofovir alafenamide + emtricitabine, or BIC/TAF/FTC (Biktarvy)
 Dolutegravir + abacavir + lamivudine, or DTG/ABC/3TC (Triumeq)
 Dolutegravir + rilpivirine, or DTG/RPV (Juluca)
 Dolutegravir + lamivudine, or DTG/3TC (Dovato)
 Elvitegravir + cobicistat + tenofovir alafenamide + emtricitabine, or

 EVG/c/TAF/FTC (Genvoya)
 Elvitegravir + cobicistat + tenofovir disoproxil fumarate + emtricitabine, or EVG/c/TDF/FTC
(Stribild)
Protease inhibitor (PI)- based:
 Atazanavir + cobicistat, or ATV/c (Evotaz)
 Darunavir + cobicistat, or DRV/c (Prezcobix)
 Darunavir + cobicistat + tenofovir alafenamide + emtricitabine, or DRV/c/TAF/FTC)
(Symtuza)
Non-nucleoside switch transcriptase inhibitor (NNRTI)- based:
 Doravirine + tenofovir disoproxil fumarate + lamivudine, or DOR/TDF/3TC (Delstrigo)
 Efavirenz + tenofovir disoproxil fumarate + emtricitabine, or EFV/TDF/FTC (Atripla)
 Rilpivirine + tenofovir alafenamide + emtricitabine , or RPV/TAF/FTC (Odefsey)
 Rilpivirine + tenofovir disoproxil fumarate + emtricitabine, or RPV/TDF/FTC (Complera)
Nucleoside/nucleotide switch transcriptase inhibitor (NRTI)- based:
 Abacavir + lamivudine, or ABC/3TC (Epzicom)
 Abacavir + lamivudine + zidovudine, or ABC/3TC/ZDV (Trizivir)
 Tenofovir alafenamide + emtricitabine, or TAF/FTC (Descovy)
 Tenofovir disoproxil fumarate + emtricitabine, or TDF/FTC (Truvada) Tenofovir disoproxil
fumarate + lamivudine, or TDF/3TC (Cimduo)
 Zidovudine + Lamivudine or ZDV/3TC (Combivir)
Descovy and Truvada have likewise been endorsed as approaches to forestall HIV disease for
individuals who are at high danger. Be that as it may, in the event that you take both of them, you need
to rehearse safe sex, as well.[14.27]
PrEP Medication
Pre-openness prophylaxis (or PrEP) is a route for individuals who don't have HIV yet who are at high
danger of getting HIV to forestall HIV contamination by taking a pill consistently. The pill (brand
name Truvada) contains two medications (tenofovir and emtricitabine) that are utilized in blend with
different meds to treat HIV. At the point when somebody is presented to HIV through sex or infusion
drug use, these medications can attempt to hold the infection back from building up a perpetual
disease.
At the point when taken day by day, PrEP is exceptionally viable for forestalling HIV. Studies have
shown that PrEP diminishes the danger of getting HIV from sex by about 99% when taken day by day.
Among individuals who infuse drugs, PrEP diminishes the danger of getting HIV by in any event 74%

when taken day by day. PrEP is substantially less successful in the event that it's anything but taken
reliably, As PrEP just secures against HIV, condoms are significant for the assurance against different
STDs. Condoms are additionally a significant counteraction system if PrEP isn't taken reliably. PrEP
drugs for HIV incorporate Truvada and Descovy.
Individuals who infuse drugs are frequently at higher danger for HIV, particularly on the off chance
that they share needles or different devices. Gay and sexually unbiased men are at higher danger from
sexual action, however hetero people can likewise get it from sexual movement.
PrEP can help secure both you and your child on the off chance that you intend to get pregnant with
HIV. It helps block the infection during pregnancy.[32]
ADVANCEMENTS IN TREATING HIV
Given the huge improvement in HIV the board by ART, the present examination for the most part
targets creating antiretroviral meds with durable impacts. In contrast to right now accessible
medications with every day dosing, the future enduring medications are relied upon to have week after
week, month to month, or even less regular dosing.
The enduring ART can be of various plans, including pills, infusions, fixes, or embeds. Likewise, to
have side effects, such details are relied upon to further develop treatment adherence and decrease
treatment-related expenses. [14]
Another significant methodology is to grow extensively killing antibodies that can work with HIV
treatment from numerous points of view. These antibodies can straightforwardly tie to the infection
and forestall their entrance to the cells; in this way, expanding the pace of infection disposal.
Also, they can trigger an invulnerable reaction in HIV-tainted cells to guarantee the
killing of the infection. Above all, the immunizer by restricting to a key viral section can frame an
intricate that can start a safe reaction like an inoculation, which in this way will assist with creating
insusceptibility against future viral experiences.
Like ART that incorporates a mix of medications, a counter acting agents based on treatment ought to
incorporate a blend of numerous antibodies or a mix of medications and antibodies. Studies directed
on monkeys have shown that a blend of corresponding antibodies can adequately smother HIV disease
for a delayed period. [9,23]
Albeit no antibody is as yet accessible to forestall HIV contamination, the advancement of remedial
immunizations that can be given to effectively tainted individuals is going on. By animating the
insusceptible framework, these immunizations will set up the body to deal with HIV disease for a
delayed period.

Additionally, the advancement of new medications for the standard every day ART is going on. A few
medications that are being scrutinized incorporate nucleoside turn around transcriptase movement
inhibitors (hinder HIV switch transcriptase and forestall DNA amalgamation) and development
inhibitors (end viral development by focusing on HIV lifecycle).
Besides, drugs that tight spot to viral surface protein (gp120) to restrain infection intervened safe cell
disease, just as medications that repress capsid (protein shell to cover viral genome) arrangement are
being scrutinized.[25]
SIDE EFFECTS OF ART DRUGS
The ART medications can have side effects, despite the fact that more current drugs generally don't
cause as many. You might have some for a brief time frame. They may include:
1. Feeling squeamish or hurling
2. Diarrhea
3. Weakness
4. Dizziness
5. Skin rashes
6. Inconvenience resting
7. Trouble sleeping
Regularly,side effects will disappear as your body changes with the medicine. On the off chance that
an side effect is troublesome, you might have the option to take care of it. Check with your drug
specialist or specialist about whether you should take your meds on a empty stomach or not. Tell your
doctor if you're experiencing difficulty. They may recommend something to help or change your
treatment routine to decrease the effect. Try not to quit taking your ART. That could allow HIV an
opportunity to get more grounded and accomplish more harm to you.
LIFESTYLE CHANGES
A good and healthy way of life can facilitate a portion of the impacts of HIV or its treatment:
 Balanced diet
Energy and supplements help your body battle HIV. A good eating routine may likewise allow your
prescriptions to work better and could ease incidental effects. In any case, be mindful so as to forestall
foodborne disease by keeping away from crude meat and eggs. [4]
 Regular exercise
It supports strength and perseverance, brings down your danger of misery, and helps your defense
mechanism work better.

 No smoking
Smoking can make you bound to get a genuine condition like malignancy, pneumonia, coronary
illness, or chronic obstructive pulmonary disease(COPD). Individuals with HIV who smoke will in
general have more limited life expectancies than the individuals who don't.
 Vaccinations
Get some information about whether they suggest that you get immunizations against pneumonia,
influenza, hepatitis A or B, or HPV.[22]
CONCLUSION
There is many research going on to find the cure of this disease but it is not yet achieved till date,
researchers claim that the best way to counter this disease is prevention. Health workers, Red Cross
society, NGOs, schools, colleges, they play an important role in exploring the myths and telling people
the facts and truth base on research and scientific explanations hence eradicating the misconception
regarding this disease. Due to complexity of HIV and its potential for resistance, ARV treatment can
immediately become troublesome for patients. Among 2018 and the present, the clinical local area has
seen a wide development of FDA-endorsed ARV treatments for the treatment of HIV. These
treatments incorporate new fixed-portion, blend tablets; new medications that work through
unexpected components in comparison to those beforehand available and surprisingly new mechanism
for already existing drugs. These new prescriptions affect current treatment rules and may help
patients live more, better lives.
REFERENCE
1. Pharmacotherapy 5th edition by Joseph.T. Dipiro, page no:2158-2161.
2. Goodman and Gilman. The Pharmacological Basis of Therapeutics page no: 1861 – 1872.
3. Clinical Pharmacy & Therapeutics byRoger walker, page no: 590 – 619.
4. Bartlett JA, Benoit SL, Johnson VA, et al. Lamivudine plus zidovudine compared with
zalcitabine plus zidovudine in patients with HIV infection. A randomized, double-blind,
placebo-controlled trial. Ann Intern Med 1996, 125: 161-72.
http://amedeo.com/lit.php?id=8686973.
5. Bernasconi E, Boubaker K, Junghans C, et al. Abnormalities of body fat distribution in HIV-
infected persons treated with antiretroviral drugs: J Acquir Immune Defic Syndr 2002, 31:50-5.
6. Blanchard JN, Wohlfeiler M, Canas A, et al. Pancreatitis treated with didanosine and tenofovir
disoproxil fumarate. Clin Infect Dis 2003; 37: e57-62.
http://amedeo.com/p2.php?id=12942419&s=hiv.

7. Bogner JR, Vielhauer V, Beckmann RA, et al. Stavudine versus zidovudine and the
development of lipodystrophy. J AIDS 2001, 27: 237-44.
8. Brinkman K, Smeitink JA, Romijn JA, Reiss P. Mitochondrial toxicity induced by nucleoside-
analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of ART-related
lipodystrophy. Lancet 1999, 354:1112-5. http://amedeo.com/lit.php?id=10509516.
9. CAESAR Co-ordinating Committee. Randomised trial of addition of lamivudine or lamivudine
plus loviride to zidovudine-containing regimens for patients with HIV-1 infection: the
CAESAR trial. Lancet 1997, 349:1413-1421. http://amedeo.com/lit.php?id=9164314
10. Carr A, Chuah J, Hudson J, et al. A randomised, open-label comparison of three HAART
regimens including two nucleoside analogues and indinavir for previously untreated HIV-1
infection: the OzCombo1 study. AIDS 2000, 14: 1171-80.
11. Carr A, Martin A, Ringland C et al. Long-term changes in lipodystrophy after switching from
thymidine analogues to abacavir. Antiviral Therapy 8:L15, 2003.
12. Carr A, Workman C, Smith DE, et al. Abacavir substitution for nucleoside analogs in patients
with HIV lipoatrophy: a randomized trial. JAMA 2002, 288:207-15.
13. Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred
zidovudine in symptom-free HIV infection. Lancet 1994, 343:871-81.
14. DeJesus E, McCarty D, Farthing CF, et al. Once-daily versus twice-daily lamivudine, in
combination with zidovudine and efavirenz, for the treatment of antiretroviral-naive adults
with HIV infection: a randomized equivalence trial. Clin Infect Dis 2004, 39:411-8.
15. Delta: a randomised double-blind controlled trial comparing combinations of zidovudine plus
didanosine or zalcitabine with zidovudine alone in HIV-infected individuals. Lancet 1996, 348:
283-91. http://amedeo.com/lit.php?id=8709686.
16. Dienstag JL, Schiff ER, Wright TL, et al. Lamivudine as initial treatment for chronic hepatitis
B in the United States. New Eng J Med 1999, 341:1256-1263, 1999.
17. Vella S, Schwartländer B, Sow SP, et al. The history of antiretroviral therapy and of its
implementation in resource-limited areas of the world. AIDS. 2012;26(10):1231-1241.
18. Arts EJ, Hazuda DJ. HIV-1 antiretroviral drug therapy. Cold Spring Harb Perspect Med.
2012;2(4):a007161.
19. Chaudhuri S, Symons JA, Deval J. Innovation and trends in the development and approval of
antiviral medicines: 1987–2017 and beyond. Antiviral Res. 2018;155:76-88.
20. Trogarzo (ibalizumab-uiyk) package insert. Montreal, Quebec: Theratechnologies Inc; March
2018.
21. Pifeltro (doravirine) package insert. Whitehouse Station, NJ: Merck & Co, Inc; March 2019.
22. Rukobia (fostemsavir) package insert. Research Triangle Park, NC: GlaxoSmithKline; July
2020.
23. Pan F, Chernew ME, Fendrick AM. Impact of fixed-dose combination drugs on adherence to
prescription medications. J Gen Intern Med. 2008;23(5):611-614.
24. Verma AA, Khuu W, Tadrous M,et al.Fixed-dose combination antihypertensive medications,
adherence, and clinical outcomes: a population-based retrospective cohort study. PLoS Med.
2018;15(6):e1002584.
25. National Institutes of Health. HIVinfo. FDA-approved HIV medicines.
hivinfo.nih.gov/understanding-hiv/fact-sheets/fda-approved-hiv-medicines. Accessed
September 22, 2020.
26. Prezista (darunavir) package insert. Titusville, NJ: Janssen Therapeutics; May 2019.
27. Truvada (emtricitabine/tenofovir disoproxil fumarate) package insert. Foster City, CA: Gilead
Sciences, Inc; June 2004/2020.
28. Delstrigo (doravirine/lamivudine/tenofovir disproxil fumerate) package insert. White House
Starion, NJ: Merck & Co, Inc; August 2018.
29. Descovy (emtricitabine/tenofovir alafenamide) package insert. Foster City, CA: Gilead
Sciences, Inc; December 2019.
30. Tivicay (dolutegravir) package insert. Research Triangle Park, NC. GlaxoSmithKline; June
2020.
31. Iacob SA, Iacob DG. Ibalizumab targeting CD4 receptors, an emerging molecule in HIV
therapy. Front Microbiol. 2017;8:2323.
32. Emu B, Fessel J, Schrader S, et al. Phase 3 study of ibalizumab for multidrug-resistant HIV-1.
N Engl J Med. 2018;379:645-654.
33. Li Z, Zhou N, Sun Y, et al. Activity of the HIV-1 attachment inhibitor BMS-626529, the active
component of the prodrug BMS-663068, against CD4-independent viruses and HIV-1
envelopes resistant to other entry inhibitors. Antimicrob Agents Chemother. 2013:57(9):4172-
4180.

34. Kozal M, Aberg J, Pialoux G. Fostemsavir in adults with multidrug-resistant HIV-1 infection.
N Engl J Med. 2020;382(13):1232-1243.
35. Cahn P, Fink V, Patterson P. Fostemsavir: a new CD4 attachment inhibitor. Curr Opin HIV
AIDS. 2018;13(4):341-345.
36. Biktarvy (bictecgravir/emtricitabine/tenofovir alafenamide) package insert. Foster City, CA:
Gilead Sceinces, Inc; February 2018.
37. Gallant J, Lazzarin A, Mills M, et al. Bictegravir, emtricitabine, and tenofovir alafenamide
versus dolutegravir, abacavir, and lamivudine for initial treatment of HIV-1 infection (GS-US-
380-1489): a double-blind, multicentre, phase 3, randomised controlled non-inferiority trial.
Lancet. 2017;390(10107):2063-2072.
38. Sax PE, Pozniak A, Montes M, et al. Coformulated bictegravir, emtricitabine, and tenofovir
alafenamide versus dolutegravir with emtricitabine and tenofovir alafenamide, for initial
treatment of HIV-1 infection (GS-US-380-1490): a randomised, double-blind, multicentre,
phase 3, non-inferiority trial. Lancet. 2017;390(10107):2073-2082.
39. Malina JM, Ward D, Brar I, et al. Switching to fixed-dose bictegravir, emtricitabine, and
tenofovir alafenamide from dolutegravir plus abacavir andlamivudine in virologically
suppressed adults with HIV-1: 48 week results of a randomised, double-blind, multicentre,
active-controlled, phase 3, non-inferiority trial. Lancet HIV. 2018;5(7):E357-E365.

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Available Online at www.ijptb.com Singh A.,et al. Int. J. Pharm. Technol. Biotechnol.

New approaches in treatment of AIDS

*Corresponding Author: Prof. (Dr) Amandeep Singh

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Fig.1: Non-Transmission of HIV

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Fig.2: Transmission of HIV

Fig.3: Electron microscopy of HIV-1 virions

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Fig.4: Genomic layout of HIV-1 and HIV-2

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 Dolutegravir and elvitegravir are accessible in the accompanying blend drugs:

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