HIV and AIDS: Pathology review
Case Study0:00–1:00
Two people come to the infectious disease clinic. The first one’s David, a 42 year old man who has a fever, associated with a cough and difficulty breathing.
David mentions that he’s HIV-positive, so you decide to run a blood test, which reveals an alarming T cell count of 180 cells / mm3.
You immediately ask for a chest X-ray, which shows gray hazy-looking areas in both lungs. Next comes Charles, a 32 year old man.
Charles was referred to the clinic by his dentist, who detected white plaques on both sides of his tongue. When you try to scrape the plaques with a tongue depressor, you realize that they can’t be removed.
Upon further questioning, Charles tells you that lately he’s been losing a ton of weight, although he hasn’t been exercising or dieting at all.
You decide to ask for an HIV-1/2 antigen/antibody immunoassay, which turns out positive.Okay, now both David and Charles have HIV, which stands for human immunodeficiency virus.
Pathology1:00–1:34
HIV specifically targets the cells of our immune system, leading to progressive immunodeficiency, which is when the immune system begins to fail gradually.
Ultimately, affected individuals can develop AIDS, or acquired immunodeficiency syndrome. What’s important to note is that AIDS puts at increased risk of certain opportunistic infections or tumors that a healthy immune system would usually be able to fend off.Now, HIV can be transmitted via certain bodily fluids from an infected person, including blood, genital fluids like semen or vaginal discharge, and breast milk.
Transmission1:34–3:07
However, HIV is not present in saliva, sweat, urine, or feces. Now, to contract the infection, these bodily fluids need to come into direct contact with a healthy person's blood, broken skin, or mucosal surfaces.
The most common means of transmission is horizontal via sexual intercourse, especially via male-to-male transmission, but also male-to-female and female-to-male transmissions can occur, while female-to-female transmission of HIV is quite rare.
The next most common means of horizontal transmission involves direct blood-to-blood contact, which, remember, is most common among intravenous drug abusers who share needles.
Less commonly, blood-to-blood contact can occur via accidental needlestick injuries, or by transfusing blood products from an infected donor.
To prevent this, blood donations are always screened for infections like HIV, among others. Finally, for your exams, you must absolutely know that HIV can also be passed via vertical transmission, which means that a pregnant individual can transmit the infection to their child before birth via the placenta, as well as during delivery via blood or genital fluids, and afterwards via breast milk.
And that’s very high yield! All right, now there are two distinct types of HIV: HIV-1 and HIV-2.
Structure3:07–4:33
Although they’re basically the same, keep in mind that HIV-1 is more common, while HIV-2 is less infectious and thus less common.
Now, regardless of the type, the viral structure is the same. HIV is a single-stranded, positive-sense, enveloped RNA retrovirus.
HIV has a diploid genome, which means the virus has two copies of positive-sense single-stranded RNA. Within this RNA, there’s the genes that contain all the necessary information to synthesize the viral enzymes and structural proteins within the infected cells.
For your exams, there are three main genes you need to remember. The first one’s the gag gene, which codes for two important structural proteins.
One is the capsid protein p24, and the other one is the matrix protein p17. Then there’s the pol gene, which codes for enzymes like reverse transcriptase, integrase, and protease, which we’ll cover in a bit.
Finally, the env gene codes for the glycoprotein gp160, which is then cleaved by the protease to form two envelope glycoproteins: gp120 and gp41.Now, once HIV enters the bloodstream, it targets CD4+ cells, which are immune cells that have this specific protein called CD4 on their membrane.
Mechanism of action4:33–7:51
For your exams, the main CD4+ cells to remember are T-helper cells and macrophages. Normally, the CD4 protein helps these cells communicate with other immune cells in order to trigger an immune response against foreign pathogens.
So this little protein is pretty important for our immune system, but it’s also HIV’s main receptor. In fact, HIV attaches to the CD4 protein via the glycoprotein gp120 found on its envelope.
But remember that this is not enough to get inside the cell; gp120 also needs to bind to a coreceptor. During early infection, the most common coreceptor that HIV uses is the membrane protein CCR5, which is typically found on T cells and macrophages.
On the other hand, during late infection, HIV tends to switch to the membrane protein CXCR4, which is mainly found on T cells.Now, for your exams, you must absolutely know that some people have a mutated CCR5 gene.
Heterozygous mutations typically result in the expression of fewer CCR5 proteins on the host cells, which makes it harder for the virus to infect them.
As a result, these individuals present with a slower disease progression. On the other hand, individuals with homozygous mutations don’t express any CCR5.
As a result, HIV can’t infect their cells, so these individuals are resistant or immune to HIV. Unfortunately, CCR5 mutations aren’t that frequent.
Now, for those without this mutation, once gp120 binds to CD4 and either CCR5 or CXCR4, the glycoprotein gp41 is exposed and anchors to the cell membrane.
This allows the viral envelope to fuse with the cell membrane, and the virus is able to inject its RNA and enzymes into the cell.
Once inside the cell, the enzyme reverse transcriptase uses this viral RNA to synthesize a complementary double-stranded piece of “proviral” DNA.
Then, this proviral DNA enters the host cell’s nucleus, where the enzyme integrase helps it integrate into the host cell’s DNA.
Pretty sneaky, huh? Ultimately, new HIV viruses are assembled and bud off from the cell membrane to infect more cells.
One important thing to be aware of is that HIV tends to make tons of errors when it replicates. As a result, the virus can rapidly acquire mutations that create various HIV strains, which contain slightly different viral enzymes and structural proteins.
Now, the reason why this is so important is that it allows the virus to evade the host’s immune response, as well as develop resistance to treatment.
And that’s a high yield fact!Okay, now if HIV infection is left untreated, it will progress over time, resulting in four clinical stages.
Acute stage7:51–9:56
The first one is the acute stage, which starts as soon as the individual gets infected. Most often, this initial or primary infection is mediated by the R5 strain of HIV, which uses the CCR5 coreceptor to infect macrophages and T cells near the infection site.
What’s important to note here is that, during this initial period, the individual is already infectious, but the virus hasn’t replicated enough to be detectable via HIV tests.
So, during this initial period of time called the window period, individuals who get tested can get a false negative result.
For your exams, remember that the window period for HIV usually lasts about 1 month, but it can range between 10 days to 3 months.
Now, during this window period, infected cells start migrating from the infection site to the lymph nodes, where a lot of immune cells live.
This leads to a big spike in HIV replication, while the T cells decline dramatically. At a certain point, the virus replicates so much that the window period ends, and HIV tests are able to detect the infection.
Now, HIV replication continues to increase until it peaks at about week 6 from the primary infection. At this point, individuals may begin to experience flu-like or mononucleosis-like symptoms, such as fever, fatigue, lymphadenopathy or swollen lymph nodes, and joint or muscle aches.
These symptoms typically last for about 2 weeks, during which the immune system mounts a counterattack, and starts to control the amount of viral replication.
As a result, the viral count declines, while the T cells rise again. This trend usually continues until month 2; during this period, the T cell count usually remains at a normal level, over 500 cells / mm3.As the virus declines, the HIV infection enters its second stage, which is the chronic or clinically latent stage.
Clinically latent stage9:56–11:17
And this stage can last anywhere between 2 to 10 years. Now, during this stage, the T cell count usually remains at a level that’s between 350 and 500 cells / mm3, so the affected individual can still fight off other infections and initially remain asymptomatic.
However, bear in mind that the virus keeps slowly replicating in the lymph nodes, while T cells gradually decrease. As a consequence, the immune system progressively weakens, and some latent or dormant infections can reactivate.
A very common one is herpes simplex virus, which causes herpes with painful oral blisters or genital ulcers and pustules; as well as varicella-zoster virus, which may lead to shingles, with painful vesicles that are typically located along one dermatome.
Another very high yield latent pathogen is mycobacterium tuberculosis, which causes a pulmonary disease called tuberculosis.
In addition, people living with HIV are more susceptible to develop community-acquired pneumonia, and for your exams, remember that the most common cause is Streptococcus pneumoniae.
Symptomatic stage11:17–13:17
Now, remember how HIV replication can create viral mutations? Well, during the clinically latent stage, some individuals may develop an X4 strain of HIV that targets the CXCR4 coreceptor, which is essentially only on T cells.
These X4 strains kind of lay low in the lymphoid tissues, and steadily destroy CD4+ T cells as the viral count increases.
That leads to the third stage of HIV infection, or the symptomatic stage. At this point, the body’s T cells drop low enough, between about 200 to 350 cells / mm3.
As a consequence, individuals become moderately immunocompromised, and may start developing relatively minor infections.
Among the most frequent ones, there’s oral thrush, also known as oral candidiasis, which is a scrapable white plaque caused by the yeast Candida albicans.
The diagnosis can be confirmed upon microscopy on a smear sample, where the most high yield finding is the presence of pseudohyphae.
This is when candida cells have an elongated shape that looks like long thin filaments. Another similar lesion is oral hairy leukoplakia, which is a hairy-looking white plaque on the side of the tongue caused by Epstein-Barr virus.
To set these two white plaques appart, the main difference is that hairy leukoplakia is unscrapable. And that’s a high yield fact!
Another characteristic condition at this stage is Kaposi sarcoma, which is a malignant tumor of the skin and soft tissues that’s caused by the human herpesvirus 8, or HHV-8.
What’s important to note is that, upon a punch biopsy, you’d find lymphocytic inflammation, meaning that the skin is infiltrated with lymphocytes.
Finally, individuals at the symptomatic stage often develop malignant lesions from infection by the human papillomavirus, or HPV.
These include squamous cell carcinoma of the anus in males and cervix in females. As the viral count continues to increase, more T cells are lost.
AIDS13:17–22:39
Ultimately, individuals reach the fourth stage of HIV infection, called AIDS, which is when the T cells fall below 200 cells / mm3.
At this point, individuals become severely immunocompromised and may present with persistent fever, fatigue, unintentional weight loss, and diarrhea.
In addition, having a T cell count below 200 cells/mm3 puts the affected individual at risk for some serious “AIDS-defining” conditions, such as certain tumors or opportunistic infections that a healthy immune system would typically be able to fend off.
Ultimately, many people with HIV infection die from these conditions. A very high yield “AIDS-defining” condition is histoplasmosis, which is caused by the fungus Histoplasma capsulatum.
Most individuals with histoplasmosis experience fever, weight loss, and fatigue, as well as cough, and dyspnea. In addition, some individuals may present with diarrhea, nausea, and vomiting.
For diagnosis, the most high yield feature seen with a peripheral blood smear are oval yeast cells within macrophages. Another AIDS-defining condition is pneumocystis pneumonia by the fungus Pneumocystis jirovecii.
This condition also presents fever, weight loss, and fatigue, as well as cough, and dyspnea. So to differentiate it from histoplasmosis, a key finding on chest imaging that should make you think of pneumocystis are “ground-glass” opacities, which are gray hazy-looking areas in the lungs.
So be sure to keep an eye out for this clue! Another very frequently tested AIDS-defining condition is progressive multifocal leukoencephalopathy, which is caused by the JC virus.
Keep in mind that JC virus can be found latent in most people, since a healthy immune system can keep it under control, but it can reactivate in case of severe immunosuppression.
Now, progressive multifocal leukoencephalopathy is a demyelinating disease that affects multiple locations of the brain and worsens over time.
Symptoms typically include progressive motor and cognitive neurologic symptoms like weakness, clumsiness due to lack of coordination, speech difficulties, and dementia.
Diagnosis of progressive multifocal leukoencephalopathy can be confirmed via MRI, where the demyelination can be spotted as non enhancing areas.
These individuals present with an altered mental status, as well as cerebral atrophy, which can be seen on neuroimaging.
But there’s more! Over time, as the T cell count falls below 100 cells/mm3, individuals become severely susceptible to opportunistic infections.
One of them is aspergillosis, a lung infection that’s caused by the fungus aspergillus fumigatus. Symptoms include hemoptysis or coughing up blood, and pleuritic chest pain, as well as fever, cough, and dyspnea.
A very high yield fact for diagnosis is that chest imaging can reveal pulmonary infiltrates and cavitation due to tissue necrosis.
Another big one is cryptococcosis. This is caused by inhaling the fungus Cryptococcus neoformans, which is typically found in soil and bird droppings.
Rarely, the infection can affect the lungs, which is known as pulmonary cryptococcosis. However, in severely immunocompromised individuals, the infection may disseminate or spread to the brain, causing cryptococcal meningitis.
Affected individuals may experience symptoms like headache and sensitivity to light, as well as nausea and vomiting. If cryptococcal meningitis is suspected, diagnosis can be confirmed using an India ink stain of the cerebrospinal fluid.
And because cryptococcus neoformans is an encapsulated yeast, this stain allows to see a clear halo around the yeast cells.
In addition, a latex agglutination test can be used to detect the characteristic polysaccharide capsular antigens. Another opportunistic infection that may hit the brain is toxoplasmosis, which is caused by the parasite Toxoplasma gondii.
Individuals usually get infected from contact with cat feces, as well as consumption of undercooked meat, especially pork and lamb.
In severely immunocompromised individuals, toxoplasma may spread to the brain, causing cerebral toxoplasmosis. This may present with a headache, fever, and neurologic symptoms like weakness, speech difficulties, and seizures.
Now, cerebral toxoplasmosis is characterized by multiple brain abscesses. So in a test question, a big clue for the diagnosis would be a CT scan or MRI showing multiple ring-enhancing lesions with central necrosis.
Moving on, another important parasite here is cryptosporidium spp, which causes cryptosporidiosis. The main symptom is chronic watery diarrhea, associated with abdominal pain.
Diagnosis can be confirmed via stool samples, showing oocysts upon acid-fast staining. Then there’s candida albicans again, but when the T cell count falls below 100, it can progress from the oral cavity to the esophagus, resulting in esophagitis.
This usually presents with dysphagia or difficulty in swallowing, odynophagia or painful swallowing, and can also lead to fever.
What’s high yield is that with upper endoscopy, you’d be able to find white plaques surrounded by erythema or reddening of the mucosa.
The diagnosis of candida esophagitis can be confirmed upon biopsy, where the most high yield finding is the presence of pseudohyphae.
Now, bear in mind that esophagitis may also be caused by cytomegalovirus or CMV. In this case, upper endoscopy may reveal large superficial linear ulcers surrounded by normal appearing mucosa.
CMV may also cause retinitis, or inflammation of the retina, where fundoscopy shows fluffy white patches called cotton-wool spots.
Finally, remember that CMV may also present with colitis, encephalitis, and pneumonia, which are inflammation of the colon, brain, and lungs, respectively.
For diagnosis, a biopsy specimen shows enlarged cells with the characteristic owl’s eye inclusion bodies within their nuclei.Another virus that makes a comeback here is Epstein Barr virus, which remember leads to oral hairy leukoplakia when cell count falls below 500.
Now, EBV also infects B cells, which are normally killed off by T cells. But with a T cell count below 100, the infected B cells are free to survive and proliferate.
This can lead to B cell lymphomas, including both Hodgkin lymphoma and non-Hodgkin lymphoma, especially Burkitt Lymphoma and primary central nervous system or CNS lymphoma.
And if there’s a single fact you must absolutely remember here is that CNS lymphoma can be detected with a CT scan or MRI, which usually show a solitary or single ring-enhancing lesion, in contrast with the multiple lesions found in cerebral toxoplasmosis.
Then, there’s bacillary angiomatosis, a severe form of cat scratch disease caused by Bartonella henselae. This bacterium leads to benign papular vascular lesions on the skin, very similar to those seen in Kaposi’s sarcoma.
To set these two apart, remember that in bacillary angiomatosis, biopsy typically shows neutrophilic inflammation, meaning that it mostly consists of neutrophils, whereas in Kaposi's sarcoma, there’s lymphocytic inflammation.
Last but not least, there’s mycobacterium avium complex, or MAC for short. This is a group of mycobacteria similar to mycobacterium tuberculosis, so they can also infect the lungs, causing nontuberculous mycobacterial lung disease.
Although this can affect people with a T cell count below 100, keep in mind that it’s particularly common when the T cell count falls below 50.
In addition, these individuals are more likely to develop disseminated infection, which can present with nonspecific systemic symptoms like fever, night sweats, and weight loss, as well as focal lymphadenitis, meaning swollen lymph nodes that are mainly on one side of the neck.
When disseminated MAC is suspected, a blood culture is necessary to confirm the diagnosis.Wow, that was a lot! To help you remember the four clinical stages of untreated HIV infection, think of the Four Fs.
The first F stands for the Flu-like symptoms characteristic of the acute stage. Then second F is when the person Feels fine during the clinically latent stage.
After that, there’s a Falling count of CD4+ T cells, which leads to the symptomatic stage. And lastly, there’s the Final crisis, where HIV infection progresses to AIDS.
Now, for your exams, you must also be able to recognize the neonatal manifestations of HIV infection, which, remember, can be passed by the mother.
The thing with neonatal manifestations is that they’re nonspecific and varied, but for your exams, be sure to remember the most high yield ones, which include generalized lymphadenopathy and oral candidiasis, as well as chronic diarrhea, failure to thrive, and developmental delay.
Neonates22:39–23:18
In addition, neonates who progress to AIDS may develop recurrent bacterial infections, as well as opportunistic infections, such as Pneumocystis jirovecii or Cytomegalovirus.Now, a real favorite for examiners is the diagnosis of HIV infection.
The first step usually involves an HIV-1/2 antigen/antibody immunoassay, which can detect both the virus directly by looking for the p24 capsid protein, as well as the antibodies that the body has made against the virus.
Diagnosis23:18–26:15
Now, this immunoassay has a very high sensitivity and specificity, so individuals who get a negative result don’t need to be further tested.
However, what’s really important to know is that a positive immunoassay result gives a presumptive diagnosis, which means that the infection is likely, but still needs to be confirmed with another test.
In the past, the confirmatory test of choice used to be Western blot, which allows to detect antibodies against HIV, but keep it mind that this is no longer recommended by the CDC.
Nowadays, the next step is to perform an HIV-1/HIV-2 antibody differentiation immunoassay, which allows to detect specific antibodies for each type.
If this immunoassay turns out positive for either or both HIV types, then the diagnosis is confirmed. On the flip side, if the result of this test is negative for both or indeterminate, then a third test is recommended: the HIV-1 Nucleic Acid Test or NAT for short.
This test can detect the virus directly by looking for its RNA. So this is it...
if it’s positive, then the person is definitely infected with HIV-1, and if it’s negative, they’re not infected by HIV-1, which means the first antigen/antibody immunoassay was a false positive.Now, once the diagnosis of HIV infection is confirmed, it is important to determine if the disease has progressed to AIDS.
To do that, you should check the T cell count, which, remember, would be lower than 200 cells / mm3, and assess for the presence of AIDS-defining conditions.
Finally, an important thing to determine is the prognosis. This is usually done via an HIV viral load test, which allows to determine the amount of viral RNA in the individual’s blood.
And higher viral loads are usually associated with poor prognosis. Now, HIV viral load tests can also be done to monitor the effect of treatment over time, in which case a decrease in viral load means the treatment is working!
Now, to diagnose HIV in newborns, bear in mind that HIV1 HIV2 Antigen / Antibody immunoassays are not reliable. That’s because maternal antibodies may have crossed the placenta during pregnancy, resulting in false positive results.
So HIV diagnosis in newborns is usually made with HIV viral load tests, and it’s confirmed when at least two tests from different blood samples are positive.Unfortunately, there’s no cure for HIV yet.
However, there are some treatment options that can help affected individuals live longer, as well as reduce the risk of transmission.
HIV therapy should be started as soon as possible at the time of diagnosis, and remember that it’s especially urgent for individuals who already present with a CD4+ cell count below 500 cells/mm3, a high viral load, or AIDS-defining conditions.
Treatment26:15–31:08
HIV therapy involves the use of antiretroviral medications, which help slow down HIV replication, giving the immune system a chance to recover and help fight off other infections more effectively.For your exams, there are four main classes of antiretrovirals.
The first and most widely used one are reverse transcriptase inhibitors, which inhibit the reverse transcriptase enzyme, preventing it from reverse-transcribing the viral RNA into proviral DNA.
Based on their structure, reverse transcriptase inhibitors can be classified into nucleoside reverse transcriptase inhibitors, or NRTIs, which include zidovudine, stavudine, lamivudine, didanosine, abacavir, and tenofovir; or non-nucleoside reverse transcriptase inhibitors, or NNRTIs, such as efavirenz and nevirapine.
The second antiretroviral class are integrase inhibitors, which inhibit the viral integrase enzyme needed to incorporate the proviral DNA into the host cell’s DNA.
Some important integrase inhibitors include raltegravir, elvitegravir, and dolutegravir, and a tip to recognize them on a test question is that they all have “tegra” in the middle.
The third class are protease inhibitors, which work by inhibiting the protease enzyme, preventing the cleavage of viral envelope glycoproteins.
Common protease inhibitors include atazanavir, darunavir, indinavir, lopinavir, saquinavir, and ritonavir - all ending in “navir”!
And the fourth antiretroviral class are entry inhibitors, which act by preventing the binding of HIV to the CD4 protein, thereby preventing its entry into the host cell.
Entry inhibitors include enfuvirtide and maraviroc. Now, a very important concept to recall here is that HIV has a tendency to acquire mutation.
So, if an individual is treated with only one antiretroviral medication, the virus can end up mutating around that medication and ultimately become resistant to it.
To prevent drug resistance, HIV is usually treated with a combination of three antiretroviral medications; this regimen is called antiretroviral therapy, or ART.
Now, when selecting the appropriate ART regimen that’s tailored to each individual, an HIV drug resistance test is recommended.
This usually involves HIV genotyping, which examines the genetic structure of the individual’s HIV strain, to determine whether it is resistant to any antiretroviral medication.
For your exam, remember that the most frequently used regimen includes two NRTIs, along with one antiretroviral of another class, which is most often an integrase inhibitor.
In general, most ART regimens are effective against both HIV-1 and -2, but bear in mind that NNRTIs and the entry inhibitor enfuvirtide are not effective against HIV-2.
With pregnant individuals who have been newly diagnosed with HIV, the course of action is pretty much the same. That means starting ART as soon as possible, which is extremely important to reduce the risk of mother-to-child transmission.
For your exams, remember that the most commonly used regimens for pregnant individuals include the NRTIs zidovudine and lamivudine, which are usually combined with an NNRTI like efavirenz.
But this isn’t the only way to prevent HIV transmission to the baby! Firstly, if a pregnant individual that’s approaching the expected due date has high or unknown viral loads, it is recommended that they get a cesarean- or C-section.
This is usually scheduled 2 weeks before their due date, to prevent the onset of spontaneous labor that would increase the risk of transmission.
After delivery, neonates are treated with zidovudine as prophylaxis during the first four to six weeks of age. In addition, breastfeeding is contraindicated, since breast milk can carry the virus.
Now, individuals who progress to AIDS should also receive prophylactic treatment to prevent certain AIDS-defining conditions.
Those with a T cell count below 200 cells/mm3 should get antibiotic prophylaxis with trimethoprim/sulfamethoxazole, against Pneumocystis jirovecii and toxoplasma.
In addition, those with a T cell count below 50 cells/mm3 should get antibiotic prophylaxis with azithromycin or clarithromycin, against mycobacterium avium complex.All right, as a quick recap… HIV is a single-stranded, positive-sense, enveloped RNA retrovirus, which can be transmitted via contact with certain body fluids, including blood, genital fluids like semen or vaginal discharge, and breast milk.
Once inside the body, HIV infects macrophages and T-helper cells using as a receptor the CD4 protein, and as a co-receptor either CCR5 or CXCR4.
Prophylaxis31:08–31:42
If untreated, HIV infection has four stages that can be remembered as the Four Fs. The first F stands for the Flu-like symptoms characteristic of the acute stage.
Then second F is when the person Feels fine during the clinically latent stage. After that, there’s a Falling count of CD4+ T cells below 500 cells / mm3, which leads to the symptomatic stage where minor infections might arise.
Recap 31:42–34:16
Finally, there’s the Final crisis, where T cells fall below 200 cells / mm3, and HIV infection progresses to AIDS. At this stage, individuals may present with fever, fatigue, unintentional weight loss, and diarrhea.
In addition, they may develop “AIDS-defining” conditions, such as certain cancers or severe opportunistic infections, and ultimately die.
For diagnosis, the first step usually involves an HIV-1/2 antigen/antibody immunoassay. A positive result gives a presumptive diagnosis that needs to be confirmed with an HIV-1/HIV-2 antibody differentiation immunoassay.
If the result is negative or indeterminate, then diagnosis should be confirmed with a HIV-1 Nucleic Acid Test. Finally, an HIV viral load test can be done to determine the prognosis and monitor the effect of treatment over time.
Treatment involves antiretroviral therapy, or ART, which combines three drugs to prevent resistance. The typical regimen includes two nucleoside reverse transcriptase inhibitors or NRTIs for short, along with one antiretroviral medication of another class, preferably an integrase inhibitor.
Other important antiretroviral classes include non-nucleoside reverse transcriptase inhibitors or NNRTIs, protease inhibitors, and entry inhibitors.
In addition to ART, individuals that progress to AIDS should get prophylactic treatment for certain AIDS-defining conditions.Now, back to our cases.
David is a 42 year old man who’s presenting with fever, cough, and dyspnea. The reason why this is concerning is that David is HIV-positive, and has a T cell count of 180 cells / mm3.
This suggests that David may have an AIDS-defining condition. The most important clue here is the chest X-ray, which revealed ground-glass opacities in both lungs.
This should guide you straight to pneumocystis pneumonia. The other individual, Charles, has white plaques on both sides of his tongue, and the fact that they’re unscrapable should immediately make you think of oral hairy leukoplakia.
This, combined with the fact that he’s been experiencing unintentional weight loss, indicate that he may have an HIV infection.
This was supported by the HIV-1/2 antigen/antibody immunoassay, which turned out positive. The next step would involve confirming the diagnosis via an HIV-1/HIV-2 antibody differentiation immunoassay or an HIV-1 Nucleic Acid Test, as well as starting Charles on the appropriate ART regimen.
Summary 34:16–35:25
is concerning is that David is hiv-positive and has a T-cell count of 180 cells per cubic millimeter. This suggests that David may have had an aids to finding condition.
The most important clue here is the chest x-ray which revealed ground glass opacities. In both lungs.
They should guide you straight to pneumocystis pneumonia. The other individual Charles has white plaques on both sides of his tongue and the fact that they're unscratchable should immediately make you think of oral hairy.
Leukoplakia. This combined with the fact that he's been experiencing unintentional weight loss, indicate that he may have an HIV infection.
This was supported by the hiv-1 and hiv-2 antigen-antibody immunoassay, which turned out positive. The Next Step would involve confirming the diagnosis via and hiv-1 and hiv-2 antibody differentiation immunoassay, or an hiv-1 nucleic acid test as well as starting Charles on the appropriate art regimen.
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