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'What are the long term effects of the Zika virus?'.This answer summarizesZika infection consequences in adults, largely mild symptoms but autoimmune Guillian-Barre syndrome in some.Tragic long term consequences of severe birth defects from Zika infection during pregnancy.Evidence from both groups bolster the notion that Zika is a neurotrophic virus.Zika Infection Consequences In AdultsWhile the Zika virus was first identified in 1947 and it might have triggered earlier outbreaks, the first such reports began to come out only from 2007 or so, too short a period of time to be certain of all of its long term effects.In most Zika outbreaks, infection in adults appeared typically mild so much so that many may not have even known they got it. Overall it appears only ~20% of Zika-infected adults show clinical symptoms, relatively mild ones such as headache, joint pain (arthralgia), rash and conjunctivitis (1).In some recent Zika virus outbreaks, particularly the one in French Polynesia in 2013-2014, some Zika-infected adults were observed to develop Guillain–Barré syndrome - Wikipedia, an autoimmune condition caused by immune system attack of the peripheral nervous system (2).Tragic Long Term Consequences To Newborns Of Zika Infection During PregnancyThe 2015-2016 Zika outbreak in Brazil made clear Zika's potentially destructive impact on the developing nervous system. Observed in the 2016-2017 Zika outbreak in Colombia as well (3) and now named Congenital Zika Syndrome, thus far it is the most consequential and devastating long term effect of Zika virus, outcome of infection of a pregnant woman and transplacental infection of the developing fetus (4, see below from 5). Zika infection during the first trimester and mother experiencing strong clinical signs of Zika infection appear to augur the greatest risk of CZS to fetus.A prominent feature of CZS observed in Brazil's Zika outbreak was Microcephaly - Wikipedia, where the baby's head is much smaller compared to babies of similar age and sex (see below from 6). This outbreak witnessed a ~20-fold increase in microcephaly incidence in this region.Even Zika-infected newborns who were apparently healthy at birth were observed to develop brain abnormalities later (see below from 7). This series of patients included several born with normal head circumference at birth who went on to have poor head growth later. Such infants had other neurological problems such as Hypertonia - Wikipedia, Dystonia - Wikipedia, Hemiparesis - Wikipedia and Epilepsy - Wikipedia as well.Arthrogryposis - Wikipedia, malformation, particularly of the hand and feet, have also been observed in CZS (see below from 8).Both microcephaly and arthrogryposis have also been observed together in CZS (see below from 4).Brain atrophy and calcifications are some of the other brain abnormalities observed in CZS. Some CZS children born without any obvious brain abnormalities went on to develop Hydrocephalus - Wikipedia (accumulation of cerebrospinal fluid in the brain) at 3 to 12 months of age (4, 9).Retina and optic nerve damage have also been observed in some CZS cases (10), which can occur even in the absence of microcephaly at birth (11).The US CDC set up the US Zika Pregnancy Registry to coordinate with state, tribal, local and territorial health departments to track Zika-related pregnancy and birth outcomes. Its most recent report (12) on pregnancy outcomes for 1297 pregnancies with suspected Zika infections reported from 44 states from December 2015 to December 2016 concluded ~1 in 10 lab-confirmed Zika infections resulted in Zika virus-associated birth defects.Analyzing the data trove since the 2015 outbreak in Brazil, several groups including the CDC have concluded there's a causality link between Zika infection and microcephaly and other birth defects (13, 14, 15), thus adding to the long list of Vertically transmitted infection - Wikipedia. However, debate on the topic in the scientific literature also continues (16, 17, 18).Definitive risk factors for CZS are still largely unknown (19). These include roles for co-infection with Dengue virus - Wikipedia and other Arbovirus - Wikipedia, genetic polymorphisms as well as differences in virulence between different Zika virus strains.Bibliography1. Petersen, Lyle R., et al. "Zika virus." New England Journal of Medicine 374.16 (2016): 1552-1563. http://www.nejm.org/doi/pdf/10.1056/NEJMra16021132. Cao-Lormeau, Van-Mai, et al. "Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study." The Lancet 387.10027 (2016): 1531-1539. http://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(16)00562-6.pdf3. Alvarado-Socarras, Jorge L., et al. "Congenital microcephaly: A diagnostic challenge during Zika epidemics." Travel medicine and infectious disease (2018). https://www.researchgate.net/profile/Alfonso_Rodriguez-Morales/publication/323268201_Congenital_microcephaly_A_diagnostic_challenge_during_Zika_epidemics/links/5a8b3ba0aca272017e639e1d/Congenital-microcephaly-A-diagnostic-challenge-during-Zika-epidemics.pdf4. Miranda-Filho, Demócrito de Barros, et al. "Initial description of the presumed congenital Zika syndrome." American journal of public health 106.4 (2016): 598-600.5. Britt, William J. "Adverse outcomes of pregnancy-associated Zika virus infection." Seminars in perinatology. WB Saunders, 2018.6. Moore, Cynthia A., et al. "Characterizing the pattern of anomalies in congenital Zika syndrome for pediatric clinicians." JAMA pediatrics 171.3 (2017): 288-295. Characterizing the Pattern of Anomalies in Congenital Zika Syndrome7. van der Linden, Vanessa. "Description of 13 infants born during October 2015–January 2016 with congenital Zika virus infection without microcephaly at birth—Brazil." MMWR. Morbidity and mortality weekly report 65 (2016). https://www.cdc.gov/mmwr/volumes/65/wr/pdfs/mm6547e2.pdf8. Aragao, M. F. V. V., et al. "Spectrum of spinal cord, spinal root, and brain MRI abnormalities in congenital Zika syndrome with and without arthrogryposis." American Journal of Neuroradiology 38.5 (2017): 1045-1053. http://www.ajnr.org/content/ajnr/38/5/1045.full.pdf9. Chimelli, Leila, et al. "The spectrum of neuropathological changes associated with congenital Zika virus infection." Acta neuropathologica 133.6 (2017): 983-999.10. Ventura, Camila V., et al. "Risk factors associated with the ophthalmoscopic findings identified in infants with presumed Zika virus congenital infection." JAMA ophthalmology 134.8 (2016): 912-918. Ophthalmoscopic Findings in Infants With Presumed Zika Virus11. Ventura, Camila V., et al. "Zika: neurological and ocular findings in infant without microcephaly." The Lancet 387.10037 (2016): 2502. http://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(16)30776-0.pdf12. Reynolds, Megan R., et al. "Vital Signs: Update on Zika Virus-Associated Birth Defects and Evaluation of All US Infants with Congenital Zika Virus Exposure-US Zika Pregnancy Registry, 2016." MMWR. Morbidity and mortality weekly report 66.13 (2017): 366-373. https://www.cdc.gov/mmwr/volumes/66/wr/pdfs/mm6613e1.pdf13. Tang, Bor Luen. "Zika virus as a causative agent for primary microencephaly: the evidence so far." Archives of microbiology 198.7 (2016): 595-601. https://link.springer.com/content/pdf/10.1007%2Fs00203-016-1268-7.pdf14. Rasmussen, Sonja A., et al. "Zika virus and birth defects—reviewing the evidence for causality." New England Journal of Medicine 374.20 (2016): 1981-1987. http://www.nejm.org/doi/pdf/10.1056/NEJMsr160433815. CDC Press Releases16. Frank, Christina, Mirko Faber, and Klaus Stark. "Causal or not: applying the Bradford Hill aspects of evidence to the association between Zika virus and microcephaly." EMBO molecular medicine (2016): e201506058. http://embomolmed.embopress.org/content/embomm/early/2016/03/10/emmm.201506058.full.pdf17. Ribeiro, Bruno Niemeyer de Freitas, et al. "Congenital Zika syndrome and neuroimaging findings: what do we know so far?." Radiologia brasileira 50.5 (2017): 314-322. http://www.scielo.br/pdf/rb/v50n5/0100-3984-rb-50-05-0314.pdf18. Joob, B., and V. Wiwanitkit. "Spinal Cord, Spinal Root, and Brain MRI Abnormalities in Congenital Zika Syndrome." American Journal of Neuroradiology 38.10 (2017): E77-E77.19. Soriano-Arandes, Antoni, et al. "What we know and what we don’t know about perinatal Zika virus infection: a systematic review." Expert review of anti-infective therapy 16.3 (2018): 243-254.Thanks for the R2A, Scott Borden.

In other words, could someone with parental history of cat allergy develop cat allergies as an adult, especially if rather than avoiding them, they've maintained sporadic contact? Does the scientific literature have an answer for this particular situation? Not clear-cut because allergies are clearly multi-factorial with genetics/family history being only one of many causative factors. Nevertheless in the case of cat allergies, several studies across many countries and age groups cautiously suggest that protection from cat allergy in adulthood shares the following featuresExposure to cats in the 1st year of life.Frequent exposure to cats from a young age.Frequent exposure to fairly high levels of environmental sources of cat allergens.In that regard, someone in contact with cats for ~1.5 hours a day would be exposed to substantial levels of cat allergens. This is also why removal of cats from homes doesn't necessarily reduce allergic symptoms (1) for two main reasons,Cat allergens are airborne and ubiquitous, i.e., found practically everywhere.Cat allergen levels are especially very high in a cat owner's home.Ambient cat allergen levels depend greatly on local cat populations, i.e., community levels of cat allergens directly reflect community levels of cat ownership. For e.g., Fel d 1 cat allergen levels are consistently high in house-dust and mattresses of European cat owners (2). High concentrations of cat allergens, specifically Fel d1, have also been found in Swedish schools (3, 4), German schools (5), US schools (6), US homes (7), New Zealand school children's clothing and primary school classrooms (8). Among such studies, cat allergen levels were only substantially lower in special allergen-avoidance Swedish day care centers (9). Thus, someone in contact with a cat for ~1.5 hours a day is also in contact with substantial amounts of cat allergens that permeate every nook and cranny of the cat owner's house, i.e., their mattress, clothing, furniture, etc. Higher and more frequent the dose of cat allergens one's exposed to, more likely to be de-sensitized.Exposure to cats from early life appears to protect adults from cat allergy. Until the 1990s the prevailing idea was that cat-allergic individuals should practice active avoidance. The narrative started to change when counter-intuitively, a 1999 Swedish study (10) first reported that children raised in a house with a cat were less likely to become allergic to cat dander proteins. Since then this phenomenon has been reported by others and even fine-tuned in terms of details. Typically, such studies test adults for cat allergen-specific immune responses (skin prick tests and blood anti-cat allergen antibodies), and detailed questionnaires gather information on frequency of cat exposure from birth. Multiple such studies across several countries thus confirmed that early life exposure to cats appears to protect adults from cat allergies:A study on 13509 adults across 15 countries (Australia, Belgium, France, Germany, Iceland, Ireland, Italy, Netherlands, New Zealand, Norway, Spain, Sweden, Switzerland, UK, US) (11).UK studies on 2502 adults (12, 13).A US study in Detroit following 270 men and 296 women from birth (14, 15) showed that those who'd had a cat at home during their 1st year of life were significantly less likely to be sensitized to cat allergens at 18 years of age.Protective effect of cat ownership is seen even in asthmatics since two French studies on adult asthmatics found earlier the exposure, stronger the protection against cat sensitization in such adults. 187 adult asthmatics and 243 controls in the 1st study (16), and 89 men and 78 women in the 2nd study (17).In fact, studies, two in the US, one on 226 children (18) and one on 38 adults (19), and one study in Sweden on 412 children (20), suggest exposure to high levels of cat allergen induces de-sensitization types of immune response to them.Another study relevant to this question is a US one which asked if decreased cat exposure increased sensitization to cat allergen, a scenario likely when children leave homes with cats and head to cat-free college dorm rooms. Of 97 college students, none developed new-onset sensitization during the course of the year-long study (21). While the study is too small to draw major conclusions, it again suggests an adult who'd been previously exposed to cats but didn't develop sensitivity/allergy is less likely to do so following a period of reduced exposure. In other words, adults exposed to cats as children are likely to stay stably de-sensitized/tolerant to cat allergens.OTOH, an European study of 6292 adults aged 20 to 44 years suggested when an adult keeps a cat for the first time, it can double their risk of cat sensitization, i.e., new-onset cat sensitization, especially if the cat is allowed in the bedroom. However, even in this study, subjects who'd had a cat during childhood seemed protected (22).Bottomline, if someone's been exposed to cats for ~1.5 hours a day frequently, they've also been exposed to high levels of cat allergens present everywhere in that cat's environment, and if they didn't develop cat allergy yet, they're unlikely to do so now, especially if they've been exposed to cats from the 1st year of life. However, a great deal of this supposition is based on this individual's accurate observations. With sporadic and short duration exposures to cats, were there never any symptoms at all or were there sometimes mild symptoms, e.g., brief bouts of stuffy/runny nose, sneezing, etc., that the individual just didn't connect to their cat exposure? This is the key question.Bibliography1. Munir, Abul Kashem M., Max Kjellman, and Bengt Björkstén. "Exposure to indoor allergens in early infancy and sensitization." Journal of allergy and clinical immunology 100.2 (1997): 177-181. http://smartguard2000.com/www.smartguard.org/images/main_1259307915/infancy2.pdf2. Heinrich, Joachim, et al. "Cat allergen level: its determinants and relationship to specific IgE to cat across European centers." Journal of allergy and clinical immunology 118.3 (2006): 674-681.3. Munir, A., et al. "The amount of the major cat (Fel d I) and dog (Can f I) allergens in dust from Swedish schools is high enough to probably cause perennial symptoms in most children with asthma who are sensitized to cat and dog." J Allergy Clin Immunol 91 (1993): 1067-1071.4. Perzanowski, Matthew S., et al. "Relevance of allergens from cats and dogs to asthma in the northernmost province of Sweden: schools as a major site of exposure." Journal of allergy and clinical immunology 103.6 (1999): 1018-1024.5. Ritz, B. R., et al. "Allergic sensitization owing to ‘second‐hand’cat exposure in schools." Allergy 57.4 (2002): 357-361. Allergic sensitization owing to ‘second-hand’ cat exposure in schools6. Abramson, Stuart L., et al. "Allergens in school settings: results of environmental assessments in 3 city school systems." Journal of School Health 76.6 (2006): 246-249.7. Arbes, Samuel J., et al. "Dog allergen (Can f 1) and cat allergen (Fel d 1) in US homes: results from the National Survey of Lead and Allergens in Housing." Journal of allergy and clinical immunology 114.1 (2004): 111-117.8. Patchett, Kathryn, et al. "Cat allergen (Fel d 1) levels on school children's clothing and in primary school classrooms in Wellington, New Zealand." Journal of allergy and clinical immunology 100.6 (1997): 755-759.9. Wickman, M., et al. "Fel d 1 and Can f 1 in settled dust and airborne Fel d 1 in allergen avoidance day-care centres for atopic children in relation to number of pet-owners, ventilation and general cleaning." Clinical and experimental allergy: journal of the British Society for Allergy and Clinical Immunology 29.5 (1999): 626. https://www.researchgate.net/profile/Gunnel_Emenius/publication/13067902_Fel_d_1_and_Can_f_1_in_settled_dust_and_airborne_Fel_d_1_in_allergen_avoidance_day-care_centres_for_atopic_children_in_relation_to_number_of_pet-owners_ventilation_and_general_cleaning/links/54ed91520cf27fbfd7727a0f.pdf10. Hesselmar, B., et al. "Does early exposure to cat or dog protect against later allergy development?." Clinical and experimental allergy: journal of the British Society for Allergy and Clinical Immunology 29.5 (1999): 611-617.11. Roost, Hans-Peter, et al. "Role of current and childhood exposure to cat and atopic sensitization." Journal of allergy and clinical immunology 104.5 (1999): 941-947.12. Custovic, Adnan, et al. "Decreased prevalence of sensitization to cats with high exposure to cat allergen." Journal of allergy and clinical immunology 108.4 (2001): 537-539.13. Custovic, Adnan, et al. "Current mite, cat, and dog allergen exposure, pet ownership, and sensitization to inhalant allergens in adults." Journal of allergy and clinical immunology 111.2 (2003): 402-407.14. Wegienka, Ganesa, et al. "Lifetime dog and cat exposure and dog‐and cat‐specific sensitization at age 18 years." Clinical & Experimental Allergy 41.7 (2011): 979-986. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3737566/pdf/nihms494834.pdf15. Erwin, E. A., et al. "The long‐term protective effects of domestic animals in the home." Clinical & Experimental Allergy 41.7 (2011): 920-922.16. Oryszczyn, M‐P., et al. "Allergy markers in adults in relation to the timing of pet exposure: the EGEA* study." Allergy 58.11 (2003): 1136-1143. http://onlinelibrary.wiley.com/doi/10.1046/j.1398-9995.2003.00314.x/epdf17. Oryszczyn, M‐P., et al. "Cat sensitization according to cat window of exposure in adult asthmatics." Clinical & Experimental Allergy 39.10 (2009): 1515-1521. https://tel.archives-ouvertes.fr/inserm-00464564/document18. Platts-Mills, Thomas, et al. "Sensitisation, asthma, and a modified Th2 response in children exposed to cat allergen: a population-based cross-sectional study." The Lancet 357.9258 (2001): 752-756.19. Renand, Amedee, et al. "Chronic cat allergen exposure induces a T H 2 cell–dependent IgG 4 response related to low sensitization." Journal of Allergy and Clinical Immunology 136.6 (2015): 1627-1635.20. Hesselmar, B., et al. "High‐dose exposure to cat is associated with clinical tolerance–a modified Th2 immune response?." Clinical & Experimental Allergy 33.12 (2003): 1681-1685.21. Erwin, Elizabeth A., et al. "Changes in cat specific IgE and IgG antibodies with decreased cat exposure." Annals of Allergy, Asthma & Immunology 112.6 (2014): 545-550.22. Olivieri, Mario, et al. "Risk factors for new-onset cat sensitization among adults: a population-based international cohort study." Journal of allergy and clinical immunology 129.2 (2012): 420-425. https://www.researchgate.net/profile/Nino_Kuenzli/publication/51877824_Risk_factors_for_new-onset_cat_sensitization_among_adults_a_population-based_international_cohort_study/links/0046352acb67cea329000000.pdfThanks for the A2A, Anonymous.

A dastardly plan! Depending on the state you are in you probably do not actually have a common law - law anymore as only these states do.According to nolo: There are only a handful of “common law marriage states”. Some of them provide for common law marriage in their statutes, while others do so through court decisions. The common law states are:Colorado—(Colo. Rev. Stat. Ann. §14-2-109.5.)Iowa—(Iowa Code Ann. §§252A.3 and 1A.)Kansas—(Kan. Stat. §§23-2502 and 23-2714.)Montana—(Mont. Code Ann. §40-1-403.)New Hampshire—(N.H. Rev. Stat. Ann. §457:39.)OklahomaRhode IslandTexas —(Tex. Fam. Code §2.401.)Utah—(Utah Code Ann. §30-1-4.5.)So you would have to be in one of those states to pull of your diabolical plan. Plus you would have to be lodged and stay lodged with your “roommate” for several years.Nolo goes on to say, whether a common law marriage exists depends on a number of factors. First and foremost, a state has to acknowledge the legitimacy of common law marriages. It if does, then the validity of the marriage will depend in large part on how the partners view the relationship, and how they act on that perception.A couple’s intent is a crucial element in determining the existence of a common law marriage. If they treat the relationship as a marriage, it’s likely they’ll meet this requirement. But that in and of itself isn’t enough. The couple has to comply with their state’s laws regulating marriage, regarding issues such as meeting the minimum age requirements, and having the soundness of mind (mental capacity) to enter into a marriage. And, of course, neither of them can be legally married to anyone else.In addition to the above, the couple have to hold themselves out to the public as being married. There are any number of ways to do this, like opening up a joint bank account, or signing a document that says you consider yourselves to be married. Using the term “spouse” when referring to each other in public, wearing wedding rings, or using the same last name are some other possibilities. In short, both your actions and words form the basis of a common law marriage.So you have to look married in order to later claim you are married and get any shot at support or what have you. It will be alimony at best as child support generally needs paternity or signing the birth certificate which is almost as good in most states.You can find more here:Which States Recognize Common Law Marriage?