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When Hiv Invades The Brain What Is The Resulting Condition

Other Digestive Tract Complications

Medical Animation: HIV and AIDS

The assessment of gastrointestinal complications is often directed by the degree of immunosuppression and the nature and duration of symptoms . Diarrhea is a common symptom in adults with HIV infection. In one sample, approximately 40 percent of patients reported at least one episode of diarrhea in the preceding month.37 HIV also directly invades various intestinal cell populations and disturbs gut motility by affecting the autonomic nervous system, leading to HIVassociated enteropathy.38 Slightly higher rates of inflammatory bowel disease have been reported in patients with HIV infection,39 although reasons for this are unclear.

HIV-Related Complications of the Gastrointestinal System

ELISA = enzyme-linked immunosorbent assay HIV = human immunodeficiency virus PCR = polymerase chain reaction.

*Listed in order from lowest to highest typical CD4 lymphocyte count.

Information from reference6.

HIV-Related Complications of the Gastrointestinal System

ELISA = enzyme-linked immunosorbent assay HIV = human immunodeficiency virus PCR = polymerase chain reaction.

*Listed in order from lowest to highest typical CD4 lymphocyte count.

Information from reference6.

Molecular Permeability Electrical Resistance And Cell Migration Across The Brain Endothelial

In order to study HIV-1 neuroinvasiveness, we constructed a human BBB model based on previous concepts with endothelial cells and extracellular matrix on the upper side and astrocytes on the lower side of a porous membrane . The extracellular matrix communicates via integrins to endothelial cells providing the signals for the formation of tight intercellular junctions . The models constructed on collagen I or IV had a relatively low permeability coefficient for the paracellular marker inulin and a relatively high electrical resistance , whereas those on fibronectin matrix had a relatively high permeability and low electrical resistance . MATRIGEL matrix did not respond to physiological ligands and was therefore not used in HIV-1 experiments. The tightness of the model also depended on in vitro passage history , the time in culture , and the number of cells planted in each insert. The permeability was related indirectly to the MW of the tracer . Madin-Darby canine kidney , a tight epithelial cell monolayer, had lower permeability , whereas choroid plexus endothelia had higher permeability compared with brain endothelial cells . The standard model for HIV experiments was therefore constructed using a combination of collagen I and fibronectin matrix with 40,000 brain endothelial cells and 40,000 astrocytes on terephthalate membrane .

Fig. 1

Blood-brain-barrier model

Epidemiology Of Neurological Hiv Disease

Studies on the prevalence of HIV among neurologic patients are sparse. The most often quoted study is the CDC study of 195,000 patients in 20 acute-care US hospitals, which found a seroprevalence of 0â13%. This was highly correlated with the seroprevalence among all patients in the hospitals . The study data was difficult to interpret as almost two-thirds of the HIV patients were previously undiagnosed. In a hospital-based study that audited HIV manifestations in medical inpatients in South Africa, the frequency of neurological involvement was 75%, with 11% pure neurological disease, and 64% neurological and non-neurological disease combined .

The paucity of this type of data is in stark contrast to established data on the global prevalence of HIV from the Joint United Nations Programme on HIV/AIDS . In 2016, the WHO estimated that 36.7 million people worldwide are infected with HIV. Sub-Saharan Africa bears the brunt of the HIV epidemic with 25.5 million infected individuals . Asia and the Pacific have 5.1 million infected people, and Latin America has 1.6 million infected people .

There are two principal subtypes of HIV, namely HIV-1 and HIV-2:

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Potential Links Between Neuropathology Of Hiv Infection And Pathogenesis Of Had

The neuropathological hallmarks of HIV infection in the brain are termed HIV encephalitis and include widespread reactive astrocytosis, myelin pallor, microglial nodules, activated resident microglia, multinucleated giant cells, and infiltration predominantly by monocytoid cells, including blood-derived macrophages. Surprisingly, measures of cognitive function do not correlate well with numbers of HIV-infected cells, multinucleated giant cells or viral antigens in CNS tissue., In contrast, increased numbers of microglia, elevated TNF- mRNA in microglia and astrocytes, evidence of excitotoxins,, , decreased synaptic and dendritic density,, and selective neuronal loss, constitute the pathologic features most closely associated with the clinical signs of HAD. Furthermore, signs of neuronal apoptosis have been linked to HAD,, , although this finding is not clearly associated with viral burden or a history of dementia. The localization of apoptotic neurons is correlated with evidence of structural atrophy and closely associated with signs of microglial activation, especially within subcortical deep gray structures, which may show a predilection for atrophy in HAD.

Figure 1

Preventive Treatment After Exposure

HIV Neurodegenerative Mechanisms Compared to Other ...

People who have been exposed to HIV from a blood splash, needlestick, or sexual contact may reduce the chance of infection by taking antiretroviral drugs for 4 weeks. These drugs are more effective when they are started as soon as possible after the exposure. Taking two or more drugs is currently recommended.

Doctors and the person who was exposed typically decide together whether to use these preventive drugs. They base the decision on the estimated risk of infection and the possible side effects of the drugs. If they do not know whether the source is infected with HIV, they consider how likely the source is to be infected. However, even when the source of the exposure is known to be infected with HIV, the risk of infection after exposure varies, depending on the type of exposure. For example, risk from a blood splash is less than that from a needlestick.

Immediately after exposure to HIV infection, what is done depends on the type of exposure:

  • If skin is exposed, it is cleaned with soap and water.

  • Puncture wounds are cleaned with antiseptic.

  • If mucous membranes are exposed, they are flushed with large amounts of water.

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Transmission Of Hiv Infection

The transmission of HIV requires contact with a body fluid that contains the virus or cells infected with the virus. HIV can appear in nearly any body fluid, but transmission occurs mainly through blood, semen, vaginal fluids, and breast milk. Although tears, urine, and saliva may contain low concentrations of HIV, transmission through these fluids is extremely rare, if it occurs at all.

HIV is not transmitted by casual contact or by close, nonsexual contact at work, school, or home. No case of HIV transmission has been traced to the coughing or sneezing of an infected person or to a mosquito bite. Transmission from an infected doctor or dentist to a patient is extremely rare.

HIV is usually transmitted in the following ways:

HIV is more likely to be transmitted if skin or a mucous membrane is torn or damagedeven if minimally.

In the United States, Europe, and Australia, HIV has been transmitted mainly through men who have sex with men and the sharing of needles among people who inject drugs, but transmission through heterosexual contact accounts for about one fourth of cases. HIV transmission in Africa, the Caribbean, and Asia occurs primarily between heterosexuals, and HIV infection occurs equally among men and women. In the United States, fewer than 25% of adults who have HIV infection are women. Before 1992, most American women with HIV were infected by injecting drugs with contaminated needles, but now most are infected through heterosexual contact.

Adaptive Immune Response To Hiv

Cellular immune response to HIV. The cellular immune response is induced upon the entry of HIV into the target cells and synthesis of viral proteins . MHC class I on the cell surface displays the intracellularly degraded HIV peptide fragments for recognition by T-cell receptors on CD8+ T cells . CD8+ T cells lyse HIV infected cells and secrete cytokines, i.e. interferon- , tumor necrosis factor , and chemokines, i.e. MIP-1 , MIP and RANTES, that inhibit virus replication and block viral entry into CD4+ T cells. Development of CD8+ T cells is crucial for control of HIV replication. This results in declining viraemia after primary infection. In the early stages of infection, CD4+ T cells lose their proliferative capacity and therefore their contribution to viral control is minor. However, during chronic infection CD4+T cells are present and secrete interleukin-2 or cytokines, such as IFN-, to control viraemia.

Figure 3.

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Through Needles Or Other Instruments

Health care workers who are accidentally pricked with an HIV-contaminated needle have about a 1 in 300 chance of contracting HIV unless they are treated as soon as possible after exposure. Such treatment reduces the chance of infection to less than 1 in 1,500. The risk increases if the needle penetrates deeply or if the needle is hollow and contains HIV-contaminated blood rather than simply being coated with blood .

Infected fluid splashing into the mouth or eyes has less than a 1 in 1,000 chance of causing infection.

Macrophages And Neuronal Injury In Had

Immunology wars: The battle with HIV

Macrophages play a pivotal role, although somewhat paradoxical, in the pathobiology of HAD., , Under steady-state conditions, mononuclear phagocytes, macrophages and microglia act as scavengers and sentinel cells, nonspecifically eliminating foreign material, and secreting trophic factors critical for maintenance of homeostasis within the CNS microenvironment., , , , These protective functions, however, can evolve into destructive ones. A number of neurotrophins are secreted by macrophages. These factors include, but are not limited to, brain-derived neurotrophic factor , insulin-like growth factor -2,-nerve growth factor , transforming growth factor beta , neurotrophin-3 and glial-derived neurotrophic factor . Clearly, a dysregulation of macrophage neurotrophic factors by viral infection and/or immune activation may occur during disease. This dysregulation may be as important as the production of neurotoxins for eliciting neuronal damage. Additionally, some neurotrophic factors are regulated by cytokines. For example, TNF- produced by immune competent microglia can play a neurotrophic role by inducing biologically active TGF-. TGF- is a protective cytokine for mammalian neurons, particularly in protection against glutamate neurotoxicity, hypoxia and gp120-mediated neural injury. This cytokine also affects long-term synaptic facilitation.

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Chorioretinitis Secondary To Opportunistic Infections

Viruses are the most common cause of infectious retinitis and/or choroiditis. Viruses are obligate intracellular parasites that can damage the retina and/or choroid, either by direct invasion or by their ability to alter the host immune system.

Cytomegalovirus is the most common cause of necrotizing retinitis in patients who are HIV positive. Varicella-zoster virus and, less commonly, HSV may cause acute retinal necrosis . This necrotizing retinitis may be unilateral or bilateral. Another form of necrotizing retinitis, progressive outer retinal necrosis , may occur in AIDS.

Common bacterial causes of retinitis in patients who are HIV positive include Treponema pallidum and Mycobacterium tuberculosis. Fungal causes of retinitis and/or choroiditis include Pseudallescheria boydii, Cryptococcus neoformans, and Histoplasma capsulatum, as well as Candida, Sporothrix, and Aspergillus species. Parasitic causes include Toxoplasma gondii and Pneumocystis jirovecii.

Taking Care Of Yourself

Experiencing the symptoms of an HIV-associated neurocognitive condition can be confusing and even frightening. One of the most important things you can do is ask for help. Do not be afraid to start a conversation with your health care provider, family, or close friends about any symptoms you may be experiencing that involve your thinking, behavior, or coordination. Seeking medical help early to find out what is causing the problem and starting treatment, if needed, is very important. People with severe HAND may need to go to a full-time assisted living facility for their own safety and well-being.

Taking effective HIV drugs to keep the virus under control is also necessary. However, people with central nervous system problems may need extra help remembering to take their medications. This is where support from family and friends may come in. You can also ask your health care provider and local AIDS service agency for help. Finally, taking your HIV drugs regularly may be the best way to treat and prevent HIV-associated brain problems.

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When Should I Call My Health Care Provider

If you notice changes in your ability to speak, focus, or concentrate, talk with your health care provider. These symptoms are common to other conditions, including other infections, depression, and nutritional deficiencies. Unusual shifts in mood or emotions and changes in social behavior also require a conversation with a health care provider. Best results are achieved with early diagnosis and treatment.

Diagnosing Hiv Infection & Aids

Approved HIV drug could ward off Alzheimers disease ...

Doctors at NYU Langone diagnose human immunodeficiency virus, known as HIV, a chronic viral infection that destroys certain infection-fighting white blood cells. If left untreated, HIV weakens the immune system, so the body is unable to fight infections and disease. When this occurs, HIV infection leads to a chronic, possibly life-threatening illness called acquired immunodeficiency syndrome, or AIDS.

HIV is transmitted through sex by sharing needles, syringes, or other equipment through contact with infected blood or through pregnancy, childbirth, or breastfeeding.

A few weeks to three months after becoming infected with HIV, many people develop intense flu-like symptoms, such as fever, fatigue, and swollen lymph nodes. They may also experience weight loss and night sweats during this initial phase. However, many people who are infected with the virus have no symptoms for 10 years or longer.

After the initial phase of an HIV infection, the disease moves into a period called clinical latency. This means the virus is developing but is producing few if any mild symptoms. Even when it causes no symptoms, the virus can be transmitted to others.

As HIV multiplies and destroys certain white blood cellsthe CD4 cells, which fight bacteria and virusesa person may develop symptoms of infection. These might include recurring fever, intense night sweats, and prolonged swelling of lymph glands in the armpits, groin, or neck. Sores in the mouth, anus, or genitals may also occur.

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The Science Of Hiv And Aids

Key Points

  • HIV stands for Human Immunodeficiency Virus, a pathogen that works by attacking the human immune system.
  • HIV specifically targets CD4 cells, the bodys principal defenders against infection, using them to make copies of themselves.
  • Antiretroviral drugs target specific stages of the HIV lifecycle to stop HIV from replicating.

Explore this page to find out more about , , and .

HIV stands for Human Immunodeficiency Virus, a pathogen that works by attacking the human immune system. It belongs to a class of viruses called retroviruses and more specifically, a subgroup called lentiviruses, or viruses that cause disease slowly. 1

HIV cannot replicate on its own, so in order to make new copies of itself, it must infect cells of the human immune system, called CD4 cells. CD4 cells are white blood cells that play a central role in responding to infections in the body. 2

Over time, CD4 cells are killed by HIV and the bodys ability to recognise and fight some types of infection begins to decline. If HIV is not controlled by treatment, the loss of CD4 cells leads to the development of serious illnesses, or opportunistic infections. In people with normal CD4 cell levels, these infections would be recognised and cleared by the immune system. 3

Germ Theory Of Disease

In Antiquity, the Greek historian Thucydides was the first person to write, in his account of the plague of Athens, that diseases could spread from an infected person to others. In his On the Different Types of Fever , the Greco-Roman physician Galen speculated that plagues were spread by “certain seeds of plague”, which were present in the air. In the Sushruta Samhita, the ancient Indian physician Sushruta theorized: “Leprosy, fever, consumption, diseases of the eye, and other infectious diseases spread from one person to another by sexual union, physical contact, eating together, sleeping together, sitting together, and the use of same clothes, garlands and pastes.” This book has been dated to about the sixth century BC.

When the Black Deathbubonic plague reached Al-Andalus in the 14th century, the Arab physicians Ibn Khatima and Ibn al-Khatib hypothesised that infectious diseases were caused by “minute bodies” and described how they can be transmitted through garments, vessels and earrings. Ideas of contagion became more popular in Europe during the Renaissance, particularly through the writing of the Italian physician Girolamo Fracastoro.Anton van Leeuwenhoek advanced the science of microscopy by being the first to observe microorganisms, allowing for easy visualization of bacteria.

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Through Blood Transfusions Or Organ Transplants

Currently, HIV infection is rarely transmitted through blood transfusions or organ transplants.

Since 1985 in most developed countries, all blood collected for transfusion is tested for HIV, and when possible, some blood products are treated with heat to eliminate the risk of HIV infection. The current risk of HIV infection from a single blood transfusion is estimated to be less than 1 in about 2 million in the United States. However, in many developing countries, blood and blood products are not screened for HIV or are not screened as stringently. There, the risk remains substantial.

HIV has been transmitted when organs from infected donors were unknowingly used as transplants. HIV transmission is unlikely to occur when corneas or certain specially treated tissues are transplanted.

Hiv And Aids Timeline


From the bleakest early days of the epidemic, Johns Hopkins has been a leader in understanding, treating and preventing HIV and AIDS. Explore 35 years of progress, here and around the world, including the nations first HIV-positive to HIV-positive organ transplants, performed at The Johns Hopkins Hospital in 2016.

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Fda Approved Dendrimer Of Aids

A tropical microbicides, first dendrimer-based drug called VivaGel® has been submitted to the US FDA as an investigational novel drug, an aqueous-based polyacrylic acid gel containing SPL7013 buffered to physiological pH, a nanoscale dendrimeric molecule that binds to viruses and stops them from affecting the bodys cells as mention in Figure 6.

Figure 6.

Progressive Outer Retinal Necrosis

PORN is a rapidly progressive, necrotizing retinitis that has been reported in patients with advanced AIDS . The most common cause is VZV reactivation, although cases secondary to HSV have also been described. The incidence of PORN is much lower than that of ARN.

Although the exact pathophysiologic mechanism for PORN has not been completely elucidated, the general consensus is that severe immunocompromise, along with a previous infection with at least VZV, are necessary. PORN also has been described in patients with severe immunocompromise secondary to chemotherapy. 71% of cases eventually develop bilateral involvement with 67% of affected eyes ultimately developing a visual acuity of no-light-perception.

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